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Vascular Calcification:Where is the Cure?
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作者 Wen-Wen Liu Mei-Lin Liu 《Chinese Medical Sciences Journal》 CAS CSCD 2024年第3期203-216,共14页
With the progress of aging,the incidence of vascular calcification(VC)gradually increases,which is correlated with cardiovascular events and all-cause death,aggravating global clinical burden.Over the past several dec... With the progress of aging,the incidence of vascular calcification(VC)gradually increases,which is correlated with cardiovascular events and all-cause death,aggravating global clinical burden.Over the past several decades,accumulating approaches targeting the underlying pathogenesis of VC have provided some possibilities for the treatment of VC.Unfortunately,none of the current interventions have achieved clinical effectiveness on reversing or curing VC.The purpose of this review is to make a summary of novel perspectives on the interventions of VC and provide reference for clinical decision-making. 展开更多
关键词 vascular calcification CLINICAL PATHOPHYSIOLOGY therapeutic strategies novel findings
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Potential efficacy and mechanism of medicinal plants on chronic kidney disease-associated vascular calcification:a review
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作者 Han-Qing Zhang Shuang Wu +8 位作者 Xin Chen Ya-Xuan Fang Qiu-Mei Lan Zi-Jun Zhou Yan-Heng Qiao Jie Li Yan-Ru Zhao Ming Pei Bo Yang 《Traditional Medicine Research》 2024年第9期21-31,共11页
Vascular calcification is a crucial risk factor that affects the incidence and mortality of cardiovascular disease in chronic kidney disease patients.Modern medicine relies on calcium-phosphorus binding agents,calcium... Vascular calcification is a crucial risk factor that affects the incidence and mortality of cardiovascular disease in chronic kidney disease patients.Modern medicine relies on calcium-phosphorus binding agents,calcium mimetics,active vitamin D,and hemodialysis to prevent and treat vascular calcification,however,their efficacy is unsatisfactory and adverse reactions often occur.Medical plant therapy can act as an integrative regulator in patients with chronic kidney disease-associated vascular calcification,which can significantly improve patients’symptoms,but its specific mechanism has not been fully elucidated yet.In this paper,we reviewed the domestic and international theoretical studies on the pathogenesis mechanism of chronic kidney disease-associated vascular calcification in recent years,summarized eight active ingredients of medicinal plants as well as four compound formulas for improving chronic kidney disease-associated vascular calcification,and explored the mechanism of action of herbal medicine,which will provide a new strategy for promoting the prevention and treatment of vascular calcification. 展开更多
关键词 chronic kidney disease chronic kidney disease-mineral and bone disorder(CKD-MBD) vascular calcification medicinal plants herbal monomers
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Arterial stiffness, vascular calcification and bone metabolism in chronic kidney disease 被引量:1
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作者 János Nemcsik István Kiss András Tislér 《World Journal of Nephrology》 2012年第1期25-34,共10页
Patients with chronic kidney disease (CKD) have an extremely poor cardiovascular outcome. Arterial stiff-ness, a strong independent predictor of survival in CKD, is connected to arterial media calcification. A huge ... Patients with chronic kidney disease (CKD) have an extremely poor cardiovascular outcome. Arterial stiff-ness, a strong independent predictor of survival in CKD, is connected to arterial media calcification. A huge number of different factors contribute to the increased arterial calcification and stiffening in CKD, a process which is in parallel with impaired bone metabolism. This coincidence was demonstrated to be part of the direct inhibition of calcifcation in the vessels, which is a counterbalancing effect but also leads to low bone turnover. Due to the growing evidence, the defnition of “CKD mineral bone disorder” was created recently, un-derlining the strong connection of the two phenomena. In this review, we aim to demonstrate the mechanisms leading to increased arterial stiffness and the up-to date data of the bone-vascular axis in CKD. We over-view a list of the different factors, including inhibitors of bone metabolism like osteoprotegerin, fetuin-A, pyro-phosphates, matrix Gla protein, osteopontin, fbroblast growth factor 23 and bone morphogenic protein, which seem to play role in the progression of vascular calcif-cation and we evaluate their connection to impaired ar-terial stiffness in the mirror of recent scientifc results. 展开更多
关键词 Arterial stiffness vascular calcification Bone metabolism Chronic kidney disease
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Significance of detection of serum HIF-1 α and β-catenin in rat model of vascular calcification in chronic kidney disease
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作者 Qi-Qi Chen Ru-Yu Tan +2 位作者 Ting-Ting Zhu Li-Ling Zhang San-Tao Ou 《Journal of Hainan Medical University》 2021年第9期16-19,共4页
Objective:To investigate the association between serum HIF-1α,β-catenin levels and the vascular calcification in the rat model of chronic kidney disease(CKD)vascular calcification.Methods:30 SD male rats were random... Objective:To investigate the association between serum HIF-1α,β-catenin levels and the vascular calcification in the rat model of chronic kidney disease(CKD)vascular calcification.Methods:30 SD male rats were randomly divided into normal control group(CON group,n=10)and CKD vascular calcification group(CKD group,n=20).Rats in calcification group were fed with adenine combined with high phosphorus diet.At the end of the 6th week,the blood and urine of the two groups were collected to detect renal function,calcium,phosphorus and 24-hour urinary protein,the renal tissue was stained with HE,the aorta of rats was stained with Von Kossa and calcium content was determined,and the levels of HIF-1α and β-catenin in serum were detected by ElISA method.Results:compared with CON group,24-hour urinary protein,blood BUN,Scr,P,Ca×P,aortic calcium content,serum HIF-1α and β-catenin levels were significantly increased and serum calcium decreased in CKD group(P<0.05);Glomerular atrophy,renal tubule dilatation and interstitial fibrosis were seen in CKD group,Von Kossa staining of calcified nodules in aorta showed more black substance deposition.The levels of serum HIF-1α,β-catenin and serum P,Ca×P were positively correlated with the content of calcium in rat aorta.Conclusion:the levels of serum HIF-1α and β-catenin are significantly increased in patients with vascular calcification in CKD,and they are significantly related to the degree of aortic calcification. 展开更多
关键词 Chronic kidney disease vascular calcification HIF-1Α Β-CATENIN
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Predictors of Vascular Calcification in Hemodialysis Patients
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作者 Said Sayed Ahmed Khamis Ahmed Ragheb Tawfeek +2 位作者 Mohammad Gamal Al Din Al-Helbawy Mohammad EL-Sayed Abdel Samea Heba Kamal Abd El Khalek 《Open Journal of Nephrology》 2021年第2期273-280,共8页
<strong>Background:</strong> The prevalence of both cardiovascular mortality and vascular calcification is much higher in patients with chronic kidney disease (CKD) than in the general population so early ... <strong>Background:</strong> The prevalence of both cardiovascular mortality and vascular calcification is much higher in patients with chronic kidney disease (CKD) than in the general population so early detection and intervention of VC may prevent or delay the progression and achieve improved patient outcomes. <strong>Objectives:</strong> To detect different predictors of vascular calcification in haemodialysis patients. <strong>Methods:</strong> This was a cross sectional observational study that included 85 patients with end stage renal disease (ESRD) on regular dialysis 47 males and 38 females ranged between 18 and 80 years old selected from Nephrology Unit, Internal Medicine Department, Menoufia University Hospital from April 2019 to May 2020. Serum calcium, phosphorus, alkhaline phosphatase, intact PTH, serum Matrix GLA protein, vitamin D and non-contrast CT for calcium scoring of femoral arteries were performed. <strong>Results:</strong> There was a significant correlation between age of the patient by years (p value 0.0001), serum calcium (p value 0.0001), phosphate (0.0001), calcium phosphate products (p value 0.0001) and alkhaline phosphatase (0.0001), and vascular calcification score detected by non-contrast CT on femoral arteries and negative correlation between serum Matrix GLA protein p value 0.0001) and the detected calcification score;the lower the MGP level the higher calcification score while there was no correlation between body mass index (BMI) (p value 0.021) intact PTH (p value 0.117), serum vitamin D level (p value 0.643), serum albumin (p value 0.643), serum haemoglobin (p value 0.257) and duration of dialysis (p value 0.260) and the detected score. Serum phosphate and calcium phosphorus product are independent risk factors for vascular calcification severity in haemodialysis patients. <strong>Conclusions:</strong> serum phosphate, calcium phosphate products are risk factors for vascular calcification while intact PTH vitamin D has no significant role in developing vascular calcification in hemodialysis patients. Matrix GLA protein was inversely correlated with vascular calcification score. 展开更多
关键词 vascular calcification Hemodialysis End Stage Renal Disease
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Correlation between Vascular Calcification and Serum Sclerostin in MHD Patients
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作者 Yangyang Zhang Shufei Zeng +18 位作者 Chen Yun Lifeng Yang Fanna Liu Guanmin Wu Taksui Wong Bo Hu Xiangnan Dong Folan Li Yu Chen Peitian Yang Aiyun Cha Huanhuan Liu Mingming Ma B.Hocher W. Pommer Huiyuan Zheng Tong Liu Zuhui Chen Lianghong Yin 《临床医学工程》 2017年第S1期27-27,共1页
Objective Investigate the correlation between serum sclerostinlevel and chronic kidney disease-mineral and bone disorder(CKD-MBD),especially vascular calcification,in maintenance hemodialysis(MHD)patients.Methods This... Objective Investigate the correlation between serum sclerostinlevel and chronic kidney disease-mineral and bone disorder(CKD-MBD),especially vascular calcification,in maintenance hemodialysis(MHD)patients.Methods This is across-sectional study,a total of 72 MHD patients were included from the first affiliated hospital of Jinan university.Measure the biochemical indicators of mineral metabolism,renal function,and serum sclerostin level by ELISA.The abdominal aorta calcification score(AACS)was assessed according to Kauppila method on lateral spine imaging using DEXA.Patients were distributed into two groups according to the level of serum sclerostin:low sclerostingroup(≤125 pg/ml)and high sclerostingroup(>125 pg/ml).Analyze the association of serum sclerostin level with the indicators of CKD-MBD.Results There was significant difference in i PTH level between high sclerost in group and low sclerost in group.Multivariate Logistic regression analysis demonstrated that dialysis duration,male and anuria were independent risk factor of high sclerostin level,and i PTH and Kt/V were protective factors.Conclusion Dialysis duration,man,anuria was independent risk factors and i PTH,Kt/V were protective factors of high serum sclerostin level in MHD patients.There was no correlation between abdominal aorta calcification and serum sclerostin level. 展开更多
关键词 Maintenance hemodialysis Mineral and bone disorder vascular calcification SCLEROSTIN
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The Pathogenesis of the Mechanism of FGF23 in Chronic Kidney Disease Patients with Vascular Calcification
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作者 Shanshan LI Wenyu GNOG +19 位作者 Sibo HUANG Lianghong YIN Bo HU Xiangnan DONG Taksui WONG Fanna LIU Yingyan LI Yueling ZHU Xin CHEN Baozhang GUAN Shengling HUANG Shuang CUI Bing YAN Hongwei HU Shaofeng HUANG Yongpin LU Shufei ZENG Chen YUN Berthold Hocher Wolfgang Pomme 《临床医学工程》 2017年第S1期49-51,共3页
Fibroblast growth factor 23(FGF23)is a protein synthesized by bone cell and the osteoblast with endocrine function.The main role of FGF23 is to regulate serum phosphorus and 1,25(OH)2 D3 levels,it also plays an import... Fibroblast growth factor 23(FGF23)is a protein synthesized by bone cell and the osteoblast with endocrine function.The main role of FGF23 is to regulate serum phosphorus and 1,25(OH)2 D3 levels,it also plays an important role in calcium and phosphorus metabolism.The role of FGF23 in renal disease is to inhibit of phosphorus reabsorption,promote urinary phosphorus excretion and maintain a stable blood phosphorus level.Patients with chronic kidney disease(CKD)have more risk to suffer cardiovascular disease(CVD)which is related to the abnormal metabolism of calcium and phosphorus.FGF23,as newly discovered cardiovascular risk marker,several studies have shown that FGF23 level associates with multiple cardiovascular risk factors in CKD patients,especially in CKD patients with vascular calcification.To explore its pathogenesis of vascular calcification in CKD patients is particularly important,and that may help to take appropriate measures to improve the prognosis of CKD patients. 展开更多
关键词 Fibroblast growth factor 23 Chronic kidney disease vascular calcification
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Vascular wall microenvironment:Endothelial cells original exosomes mediated melatonin-suppressed vascular calcification and vascular ageing in a m6A methylation dependent manner
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作者 Su-Kang Shan Xiao Lin +18 位作者 Feng Wu Chang-Chun Li Bei Guo Fu-Xing-Zi Li Ming-Hui Zheng Yi Wang Qiu-Shuang Xu Li-Min Lei Ke-Xin Tang Yun-Yun Wu Jia-Yue Duan Ye-Chi Cao Yan-Lin Wu Chang-Ming Tan Zi-Han Liu Zhi-Ang Zhou Xiao-Bo Liao Feng Xu Ling-Qing Yuan 《Bioactive Materials》 SCIE CSCD 2024年第12期52-67,共16页
Vascular calcification and vascular ageing are“silent”diseases but are highly prevalent in patients with end stage renal failure and type 2 diabetes,as well as in the ageing population.Melatonin(MT)has been shown to... Vascular calcification and vascular ageing are“silent”diseases but are highly prevalent in patients with end stage renal failure and type 2 diabetes,as well as in the ageing population.Melatonin(MT)has been shown to induce cardiovascular protection effects.However,the role of MT on vascular calcification and ageing has not been well-identified.In this study,the aortic transcriptional landscape revealed clues for MT related cell-to-cell communication between endothelial cells(ECs)and vascular smooth muscle cells(VSMCs)in vascular calcification and vascular ageing.Furthermore,we elucidated that it was exosomes that participate in the information transportation from ECs to VSMCs.The exosomes secreted from melatonin-treated ECs(MT-ECs-Exos)inhibited calcification and senescence of VSMCs.Mechanistically,miR-302d-5p was highly enriched in MT-ECs-Exos,while depletion of miR-302d-5p blocked the ability of MT-ECs-Exos to suppress VSMC calcification and senescence.Notably,Wnt3 was a bona fide target of miR-302d-5p and modulated VSMC calcification and senescence.Furthermore,we found that maturation of endothelial derived exosomal miR-302d-5p was promoted by WTAP in an N^(6)-methyladenosine(m^(6)A)-dependent manner.Interestingly,MT alleviated vascular calcification and ageing in 5/6-nephrectomy(5/6 NTP)mice,a chronic kidney disease(CKD)induced vascular calcification and vascular ageing mouse model.MT-ECs-Exos was absorbed by VSMCs in vivo and effectively prevented vascular calcification and ageing in 5/6 NTP mice.ECs-derived miR-302d-5p mediated MT induced anti-calcification and anti-ageing effects in 5/6 NTP mice.Our study suggests that MT-ECs-Exos alleviate vascular calcification and ageing through the miR-302d-5p/Wnt3 signaling pathway,dependent on m^(6)A methylation. 展开更多
关键词 MELATONIN vascular calcification vascular ageing EXOSOMES N6-methyladenosine
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Vascular Calcification: Current Genetics Underlying This Complex Phenomenon 被引量:8
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作者 Nonanzit Perez-Hernandez Gad Aptilon-Duque +5 位作者 Ruben Blachman-Braun Gilberto Vargas-Alarcon Adrian Asael Rodriguez-Cortes Shely Azrad-Daniez Rosalinda Posadas-Sanchez Jose Manuel Rodriguez-Perez 《Chinese Medical Journal》 SCIE CAS CSCD 2017年第9期1113-1121,共9页
Objective: Vascular calcification is the consequence of the complex interaction between genetic, environmental, and vascular factors, which ultimately lead to the deposition of calcium in the tunica intima (atherosc... Objective: Vascular calcification is the consequence of the complex interaction between genetic, environmental, and vascular factors, which ultimately lead to the deposition of calcium in the tunica intima (atherosclerotic calcification) or tunica media (M6nckenberg's sclerosis). Vascular calcification is also closely related to other pathologies, such as diabetes mellitus, dyslipidemia, and chronic kidney disease. It has been concluded that the degree of vascular calcification may vary from person to person, even if the associated pathologies and environmental factors are the same. Therefore, this suggests an important genetic contribution to the development of vascular calcification. This review aimed to find the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways. Data Sources: We conducted an exhaustive search in Scopus, EBSCO, and PubMed with the keywords "genetics and vascular calcification", "molecular pathways, genetic and vascular calcification" and included the main articles from January 1995 up to August 2016. We focused on the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways. Study Selection: The most valuable published original and review articles related to our objective were selected. Results: Vascular calcification is a multifactorial disease; thus, its pathophysiology cannot be explained by a single specific factor, rather than by the result of the association of several genetic variants, molecular pathway interactions, and environmental factors that promote its development. Conclusion: Although several molecular aspects of this mechanism have been elucidated, there is still a need for a better understanding of the factors that predispose to this disease. 展开更多
关键词 ATHEROSCLEROSIS Cardiovascular Risk GENETICS POLYMORPHISMS vascular calcification
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Nano-hydroxyapatite accelerates vascular calcification via lysosome impairment and autophagy dysfunction in smooth muscle cells 被引量:8
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作者 Qi Liu Yi Luo +7 位作者 Yun Zhao Pingping Xiang Jinyun Zhu Wangwei Jing Wenjing Jin Mingyao Chen Ruikang Tang Hong Yu 《Bioactive Materials》 SCIE 2022年第2期478-493,共16页
Vascular calcification(VC)is a common characteristic of aging,diabetes,chronic renal failure,and atherosclerosis.The basic component of VC is hydroxyapatite(HAp).Nano-sized HAp(nHAp)has been identified to play an esse... Vascular calcification(VC)is a common characteristic of aging,diabetes,chronic renal failure,and atherosclerosis.The basic component of VC is hydroxyapatite(HAp).Nano-sized HAp(nHAp)has been identified to play an essential role in the development of pathological calcification of vasculature.However,whether nHAp can induce calcification in vivo and the mechanism of nHAp in the progression of VC remains unclear.We discovered that nHAp existed both in vascular smooth muscle cells(VSMCs)and their extracellular matrix(ECM)in the calcified arteries from patients.Synthetic nHAp had similar morphological and chemical properties as natural nHAp recovered from calcified artery.nHAp stimulated osteogenic differentiation and accelerated mineralization of VSMCs in vitro.Synthetic nHAp could also directly induce VC in vivo.Mechanistically,nHAp was internalized into lysosome,which impaired lysosome vacuolar H+-ATPase for its acidification,therefore blocked autophagic flux in VSMCs.Lysosomal re-acidification by cyclic-3′,5′-adenosine monophosphate(cAMP)significantly enhanced autophagic degradation and attenuated nHAp-induced calcification.The accumulated autophagosomes and autolysosomes were converted into calcium-containing exosomes which were secreted into ECM and accelerated vascular calcium deposit.Inhibition of exosome release in VSMCs decreased calcium deposition.Altogether,our results demonstrated a repressive effect of nHAp on lysosomal acidification,which inhibited autophagic degradation and promoted a conversion of the accumulated autophagic vacuoles into exosomes that were loaded with undissolved nHAp,Ca^(2+),Pi and ALP.These exosomes bud off the plasma membrane,deposit within ECM,and form calcium nodules.Vascular calcification was thus accelerated by nHAP through blockage of autophagic flux in VSMCs. 展开更多
关键词 NANO-HYDROXYAPATITE vascular calcification AUTOPHAGY LYSOSOME EXOSOME
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Protection Effect of Exogenous Fibroblast Growth Factor 21 on the Kidney Injury in Vascular Calcification Rats 被引量:4
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作者 Yu-Chen Shi Wei-Wei Lu +6 位作者 Yue-Long Hou Kun Fu Feng Gan Shu-Juan Cheng Shao-Ping Wang Yong-Fen Qi Jing-Hua Liu 《Chinese Medical Journal》 SCIE CAS CSCD 2018年第5期532-538,共7页
Background: Chronic kidney disease (CKD) is closely related to the cardiovascular events in vascular calcification (VC). However, little has known about the characteristics of kidney injury caused by VC. Fibrobla... Background: Chronic kidney disease (CKD) is closely related to the cardiovascular events in vascular calcification (VC). However, little has known about the characteristics of kidney injury caused by VC. Fibroblast growth factor 21 (FGF21 ) is an endocrine thctor, which takes part in various metabolic actions with the potential to alleviate metabolic disorder diseases, Even FGF21 has been regarded as a biomarker in CKD, the role of FGF21 in CKD remains unclear. Therefore, in this study, we evaluate the FGF21 on the kidney injury in VC rats. Methods: The male Sprague-Dawley rats were divided into three groups: ( 1 ) control group, (2) Vitamin D3 plus nicotine (VDN)-induced VC group, (3) FGF21-treated VDN group. After 4 weeks, the rats were killed and the blood was collected for serum creatinine, urea nitrogen, calcium, and phosphate measurement. Moreover, the renal tissues were homogenized for alkaline phosphatases (ALPs) activity and calcium content. The levels of FGF21 protein were measured by radioimmunoassay. The levels of β-Klotho and FGF receptor 1 (FGFR1) protein were measured by enzyme-linked immunosorbent assay (EL1SA). The structural damage and calcifications in aortas were stained by Alizarin-red S. Moreover, the structure of kidney was observed by hematoxylin and eosin staining. Results: The renal lhnction impairment caused by VDN modeling was ameliorated by FGF21 treatment, inhibited the elevated serum creatinine and urea level by 20.5% (34.750 ± 4.334 pmol/L vs. 27.630± 2.387pamol/L) and 4.0% (7.038 ± 0.590 mmol/L vs. 6.763 ±0.374 mmol/L; P 〈 0.01 ), respectively, together with the structural damages of glomerular atrophy and renal interstitial fibrosis. FGF21 treatment downregulated the ALP activity, calcium content in the kidney of VC rats by 42.1% (P 〈 0.01 ) and 11.7% (P 〈 0.05) as well as ameliorated the aortic injury and calcification as compared with VDN treatment alone group, indicating an ameliorative effect on VC. EL1SA assays showed that the expression of [3-Klotho, a component of FGF21 receptor system was increased in VDN-treated VC rats by 37.4% (6.588 ± 0.957 pg/mg vs. 9.054 ± 0.963 pg/mg; P 〈 0.01), indicating an FGF2 l-resistant state. Moreover, FGF21 treatment downregulated the level of β-Klotho in renal tissue by 16.7% (9.054 ± 0.963 pg/mg vs. 7.544± 1.362 pg/mg, P 〈 0.05). However, the level of FGFR1, the receptor of FGF21, kept unchanged under VDN and VDN plus FGF21 administration (0.191 ± 0.0376 rig/rag vs. 0.189 ± 0.032 ng/mg rs. 0.181± 0.034 mg/mg; P 〉 0.05). Conclusions: In the present study, FGF21 was observed to ameliorate the kidney injury in VDN-induced VC rats. FGF21 might be a potential therapeutic factor in CKD by cutting offthe vicious circle between VC and kidney injury. 展开更多
关键词 CHRONIC Fibroblast Growth Factor 21 Renal Insufficiency vascular calcification β-Klotho
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Beneficial effect of berberine on atherosclerosis based on attenuating vascular inflammation and calcification 被引量:2
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作者 Xiao-ming LI Qing-zhu WANG Lei GUO 《中国药理学与毒理学杂志》 CAS CSCD 北大核心 2017年第10期993-994,共2页
OBJECTIVE To investigate the beneficial effect of berberine(BBR)on atherosclerosisin Apo^(-/-) E mice and explore the underlying mechanisms based on attenuating vascular inflammation and modulating calcification in hu... OBJECTIVE To investigate the beneficial effect of berberine(BBR)on atherosclerosisin Apo^(-/-) E mice and explore the underlying mechanisms based on attenuating vascular inflammation and modulating calcification in human umbilical vein endothelial cells(HUVECs) and smooth muscle cells(SMCs).METHODS 48 Apo-/-E mice,at 6-8 weeks old,were randomly allocated into 4 groups:normal,model,bbr and atorvastatin(positive control) groups with 12 mice in each group.They were fed with high-fat diet for 4 weeks except those in Normal group and then treated with indicated drugs orsolvent for another 4 weeks.The morphology and inflammation infiltration of aortic were examined with HE staining.The expression of BMP-2 in aortic was examined by immumohistochemical staining.Blood lipid levels were examined by automatic biochemical analyzer.The expression of IL-6,TNF-α and BMP-2 in serum and tissues was detected by ELISA method.The expression of ALP and the content of calcium were detected by commercially-available kits.HUVEC cells were stimulated with TNF-α and incubated with various concentrations of BBR for 24 h.The contents of intercellular cell adhesion molecule-1(ICAM-1),vascular cell adhesion molecule(VCAM-1),matrix metalloprotein-9(MMP-9) in the culture supernatant were detected by ELISA method.Calcification was induced with β-glycerophosphatein SMC cells and the effect of BBR on the content of calcium was examined.RESULTS 4-week berberine treatment markedly lowered serum TC and LDL-c levels and improved the plaque stability in Apo-/-E mice fed with a high-fat diet(P<0.05 or P<0.01) which was comparable with the effect of atorvastatin.Berberineal so significantly decreased the levels of IL-6 and TNF-α in mice serum and aortic tissues(P<0.05 or P<0.001).Berberine tended to decrease ALP,BMP-2 levels and the content of calcium in mice serum and aortic tissues(P<0.05,P<0.01 or P<0.001) which were not observed in atorvastatin group.Berberine significantly lowered the levels of ICAM-1,VCAM-1,and MMP-9 in TNF-α-stimulated HUVECs.It can also lowered the content of calcium in SMCs.CONCLUSION BBR can profitably regulate the levels of blood lipid in mice fed with a high-fat diet,decrease the injury caused by inflammation,and attenuate vascular calcification.It may improve atherosclerosis and play a role in cardiovascular protection. 展开更多
关键词 BERBERINE ATHEROSCLEROSIS vascular endothelium INFLAMMATION vascular calcification
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Does treatment with statins have the potential of enhancing vascular calcification?
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作者 ZHANG Ming LI Xu-ping +2 位作者 QIAO Yan NIE Shao-ping MA Chang-sheng 《Chinese Medical Journal》 SCIE CAS CSCD 2008年第5期473-474,共2页
Vascular calcification is commonly found in atherosclerosis and recognized as a marker of atherosclerotic plaque burden. Many evdiences have demonstrated that vascular calcification is an active process and can be see... Vascular calcification is commonly found in atherosclerosis and recognized as a marker of atherosclerotic plaque burden. Many evdiences have demonstrated that vascular calcification is an active process and can be seen in all stages of development and intimately associated with atherosclerosis. The correlation between coronary calcifications and subclinical atherosclertotic disease has been well-known for some years. Bone morphogenetic protein-2 (BMP-2) has significant importance in bone development and the development of a wide array of tissues outside of bone. Zhang et al3,4 found mice genetically engineered to be deficient in BMP-2 die between days 7 and 10 of gestation of cardiac defects before bone formation. Many evidences have also confirmed that BMP-2 is a strong basic causative factor in vascular calcification and has been most frequently associated with calcific arteriopathy. Statins are the most powerful cholesterol-lowering drugs available. Although a major beneficial effect of statins in clinical studies is related to a marked reduction in low density lipoprotein (LDL) cholesterol levels, there are good evidences that statins hold multiple vascular protective effects,5 however, the effects of statins therapy in vascular calcification are more complex and less defined. The currently available reports of clinical trials about statins therapy of vascular calcification appeared to be paradoxical. 展开更多
关键词 STATINS vascular calcification bone morphogenetic protein-2
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Effects of Vitamin K-1 and Menaquinone-7 on Vascular Function and Blood Pressure in Warfarin-Induced Calcification-Model in Rats
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作者 Aino Siltari Niko Wickholm +5 位作者 Anne SKivimaki Kaisa Olli Krista Salli Kirsti Tiihonen Riitta Korpela Heikki Vapaatalo 《Pharmacology & Pharmacy》 2014年第12期1095-1105,共11页
Given that vascular calcification is inversely correlated with the clinical intake of menaquinone, a rat model of warfarin-induced calcification may be useful for testing menaquinone and vitamin K-1 potential effects ... Given that vascular calcification is inversely correlated with the clinical intake of menaquinone, a rat model of warfarin-induced calcification may be useful for testing menaquinone and vitamin K-1 potential effects on vascular function. The aim of the present study was to investigate effects of vitamin K-1 and menaquinone-7 treatments on blood pressure and vascular function in warfarin-induced vascular calcification model during five-week intervention in normotensive Wistar-Kyoto rats. Blood pressure was measured weekly, and at the end of the intervention in vitro vascular reactivity measurements were done. Alizarin Red S and von Kossa stainings were used to record possible calcification of aortic sections. Routine clinical chemistry was done from serum and urine samples. Vascular calcification was seen only in a few warfarin-treated animals in histological staining. Warfarin-treatment did not change significantly blood pressure of the rats. Warfarin-treatment increased slightly the endothelium-dependent relaxation of aorta after the L-type calcium channels were blocked. Also the vascular relaxation improved after NOS inhibition in the aorta of the healthy controls and menaquinone-7 treated animals, indicating that the relaxation in those groups was not totally dependent on NO. Clinical chemistry from serum showed some differences in urea, creatinine as well as lipid and glucose metabolism between the healthy controls and warfarin-treated rats. 展开更多
关键词 vascular calcification Vitamin K-1 Menaquinone-7 Blood Pressure vascular Function
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Correlation between Wnt Signalling Inhibitors (Dickkopf-1 & Sclerostin) and the Intimal Medial Thickness in Children on Maintenance Hemodialysis
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作者 Manal Abd El-Salam Mohamed Hamdi Ali +2 位作者 Nadia Youssef Riad Rasha Abd El Samad Fawaz Shima Mohamed 《Open Journal of Nephrology》 2024年第3期397-412,共16页
Background: Wnt signalling inhibitors (Dickkopf-1 and Sclerostin) signalling play a role in vascular development and may contribute to calcification. Aim: To investigate the association between Dickkopf-1 and sclerost... Background: Wnt signalling inhibitors (Dickkopf-1 and Sclerostin) signalling play a role in vascular development and may contribute to calcification. Aim: To investigate the association between Dickkopf-1 and sclerostin serum concentrations in children undergoing maintenance hemodialysis with intimal medial thickness and peak systolic velocity of the main arteries. Patients and Methods: A study was conducted on 40 children undergoing maintenance hemodialysis and controls of the same age and sex. The study measured the initial medial thickness (IMT) and peak systolic velocity (PSV) of the main vessels (carotid, ulnar, and femoral). Dickkopf-1 and sclerostin serum levels in both groups were assessed, and a routine investigation was performed. Results: The findings indicate that the levels of serum Dickkopf-1 and Sclerostin were significantly higher in the hemodialysis group 2540.65 (2215.4 - 2909.2 pg/ml) and 1.17 (0.85 - 2.03 ng/ml)respectively (P = 0.001), compared to their control group it was 1110.45 (885.45 - 1527.65 pg/ml) and 0.28 (0.25 - 0.32 ng/ml)) respectively P = 0.001. Additionally, there was a significant increase in intima-media thickness (IMT) with a decrease in peak systolic velocity (PSV) in the main blood vessels, including the carotid, ulnar, and femoral arteries. A significant correlation was also observed between Dickkopf-1 and sclerostin levels and IMT of the carotid, ulnar, and femoral arteries. Conclusion: Wnt signalling inhibitors (Dickkopf-1 and Sclerostin) exert effects beyond the bone and significantly contribute to early vascular calcification in pediatric patients undergoing maintenance hemodialysis. 展开更多
关键词 Wnt Signalling vascular calcification HEMODIALYSIS CHILDREN
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Significant roles of anti-aging protein klotho and fibroblast growth factor23 in cardiovascular disease 被引量:9
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作者 Hong-Ying DING Hou-Xun MA 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2015年第4期439-447,共9页
The klotho gene has been identified as an aging suppressor that encodes a protein involved in cardiovascular disease (CVD). The inac- tivation of the klotho gene causes serious systemic disorders resembling human ag... The klotho gene has been identified as an aging suppressor that encodes a protein involved in cardiovascular disease (CVD). The inac- tivation of the klotho gene causes serious systemic disorders resembling human aging, such as atherosderosis, diffuse vascular calcification and shortened life span. Klotho has been demonstrated to ameliorate vascular endothelial dysfunction and delay vascular calcification. Fur- thermore, klotho gene polymorphisms in the human are associated with various cardiovascular events. Recent experiments show that klotho may reduce transient receptor potential canonical6 (TRPC6) channels, resulting in protecting the heart from hypertrophy and systolic dys- function. Fibroblast growth factor23 (FGF23) is a bone-derived hormone that plays an important role in the regulation of phosphate and vi- tamin D metabolism. FGF23 accelerates urinary phosphate excretion and suppresses 1,25-dihydroxy vitaminD3 (1,25(OH)2D3)synthesis in the presence ofFGF receptorl (FGFR1) and its co-receptor ldotho, principally in the kidney. The hormonal affects of circulating klotho pro- tein and FGF23 on vascular and heart have contributed to an understanding of their roles in the pathophysiology of arterial stiffness and left ventricular hypertrophy. Klotho and FGF23 appear to play a critical role in the pathogenesis of vascular disease, and may represent a novel potential therapeutic strategy for clinical intervention. 展开更多
关键词 Cardiac hypertrophy CARDIOvascular Fibroblast growth factor23 Gene polymorphisms KLOTHO vascular calcification
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Implications of Klotho in vascular health and disease 被引量:4
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作者 Ernesto Martín-Núez Javier Donate-Correa +2 位作者 Mercedes Muros-de-Fuentes Carmen Mora-Fernández Juan F Navarro-González 《World Journal of Cardiology》 CAS 2014年第12期1262-1269,共8页
Cardiovascular disease(CVD) is a prevalent condition in general population and the first cause of death overall. Klotho, a pleiotropic protein related to longevity that acts as a co-receptor of the fibroblast growth f... Cardiovascular disease(CVD) is a prevalent condition in general population and the first cause of death overall. Klotho, a pleiotropic protein related to longevity that acts as a co-receptor of the fibroblast growth factor 23, has been proposed as a key regulator of the development of CVD. In the few clinical studies made, it has been observed a relationship between low levels of soluble Klotho and the occurrence and severity of CVD, as well as a reduction of cardiovascular risk when they are high. Also, different polymorphisms of human Klotho gene have been related to the incidence of cardiovascular events. Moreover, several experimental studies indicate that this protein acts in the maintenance of vascular homeostasis. Klotho improves endothelial dysfunction through promotion of NO production and mediates antiinflammatory and anti-aging effects such as suppression of adhesion molecules expression, attenuation of nuclear factor-kappa B or inhibition of Wnt signaling. Furthermore,this protein is related to the attenuation of vascular calcification as well as prevention of cardiac hypertrophy. The expression of this protein in the vascular wall implies a new scenario for the treatment of vascular disorders. The purpose of this review is to provide an overview of the relationship between the Klotho protein and CVD, in addition to its role in the maintenance of functional vascular integrity. 展开更多
关键词 KLOTHO Cardiovascular disease vascular health AGING Endothelial dysfunction vascular calcification
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Insulin resistance is associated with subclinical vascular disease in humans 被引量:19
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作者 María M Adeva-Andany Eva Ameneiros-Rodríguez +2 位作者 Carlos Fernández-Fernández Alberto Domínguez-Montero Raquel Funcasta-Calderón 《World Journal of Diabetes》 2019年第2期63-77,共15页
Insulin resistance is associated with subclinical vascular disease that is not justified by conventional cardiovascular risk factors,such as smoking or hypercholesterolemia.Vascular injury associated to insulin resist... Insulin resistance is associated with subclinical vascular disease that is not justified by conventional cardiovascular risk factors,such as smoking or hypercholesterolemia.Vascular injury associated to insulin resistance involves functional and structural damage to the arterial wall that includes impaired vasodilation in response to chemical mediators,reduced distensibility of the arterial wall(arterial stiffness),vascular calcification,and increased thickness of the arterial wall.Vascular dysfunction associated to insulin resistance is present in asymptomatic subjects and predisposes to cardiovascular diseases,such as heart failure,ischemic heart disease,stroke,and peripheral vascular disease.Structural and functional vascular disease associated to insulin resistance is highly predictive of cardiovascular morbidity and mortality.Its pathogenic mechanisms remain undefined.Prospective studies have demonstrated that animal protein consumption increases the risk of developing cardiovascular disease and predisposes to type 2 diabetes(T2D)whereas vegetable protein intake has the opposite effect.Vascular disease linked to insulin resistance begins to occur early in life.Children and adolescents with insulin resistance show an injured arterial system compared with youth free of insulin resistance,suggesting that insulin resistance plays a crucial role in the development of initial vascular damage.Prevention of the vascular dysfunction related to insulin resistance should begin early in life.Before the clinical onset of T2D,asymptomatic subjects endure a long period of time characterized by insulin resistance.Latent vascular dysfunction begins to develop during this phase,so that patients with T2D are at increased cardiovascular risk long before the diagnosis of the disease. 展开更多
关键词 DIABETES Cardiovascular risk Arterial stiffness Arterial elasticity Intimamedia thickness vascular calcification Insulin resistance Animal protein Vegetable protein
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Prognostic value of coronary artery calcium score in patients with stable an-gina pectoris after percutaneous coronary intervention 被引量:10
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作者 Fang-Fang WANG Jiang-Li HAN +4 位作者 Rong HE Xiang-Zhu ZENG Fu-Chun ZHANG Li-Jun GUO Wei GAO 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2014年第2期113-119,共7页
Objectives To evaluate the prognostic value of the coronary artery calcium (CAC) score in patients with stable angina pectoris (SAP) who underwent percutaneous coronary intervention (PCI). Methods A total of 334... Objectives To evaluate the prognostic value of the coronary artery calcium (CAC) score in patients with stable angina pectoris (SAP) who underwent percutaneous coronary intervention (PCI). Methods A total of 334 consecutive patients with SAP who underwent first PCI following multi-slice computer tomography (MSCT) were enrolled from our institution between January 2007 and June 2012. The CAC score was calculated according to the standard Agatston calcium scoring algorithm. Complex PCI was defined as use of high pressure bal-loon, kissing balloon and/or rotablator. Procedure-related complications included dissection, occlusion, perforation, no/slow flow and emer-gency coronary artery bypass grafting. Main adverse cardiac events (MACE) were defined as a combined end point of death, non-fatal myo-cardial infarction, target lesion revascularization and rehospitalization for cardiac ischemic events. Results Patients with a CAC score〉300 (n=145) had significantly higher PCI complexity (13.1%vs. 5.8%, P=0.017) and rate of procedure-related complications (17.2%vs. 7.4%, P=0.005) than patients with a CAC score≤300 (n=189). After a median follow-up of 22.5 months (4-72 months), patients with a CAC score≤300 differ greatly than those patients with CAC score&gt;300 in cumulative non-events survival rates (88.9 vs. 79.0%, Log rank 4.577, P=0.032). After adjusted for other factors, the risk of MACE was significantly higher [hazard ratio (HR):4.3, 95%confidence inter-val (95%CI):2.4-8.2, P=0.038] in patients with a CAC score〉300 compared to patients with a lower CAC score. Conclusions The CAC score is an independent predictor for MACE in SAP patients who underwent PCI and indicates complexity of PCI and proce-dure-related complications. 展开更多
关键词 Angina Coronary angiography Multi-slice computed tomography Heart catheterization vascular calcification
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Why do young people with chronic kidney disease die early? 被引量:12
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作者 Shankar Kumar Richard Bogle Debasish Banerjee 《World Journal of Nephrology》 2014年第4期143-155,共13页
Cardiovascular disease poses the greatest risk of premature death seen among patients with chronic kidney disease(CKD).Up to 50% of mortality risk in the dialysis population is attributable to cardiovascular disease a... Cardiovascular disease poses the greatest risk of premature death seen among patients with chronic kidney disease(CKD).Up to 50% of mortality risk in the dialysis population is attributable to cardiovascular disease and the largest relative excess mortality is observed in younger patients.In early CKD,occlusive thrombotic coronary disease is common,but those who survive to reach end-stage renal failure requiring dialysis are more prone to sudden death attributable mostly to sudden arrhythmic events and heart failure related to left ventricular hypertrophy,coronary vascular calcification and electrolyte disturbances.In this review,we discuss the basis of the interaction of traditional risk factors for cardiovascular disease with various pathological processes such as endothelial dysfunction,oxidative stress,low grade chronic inflammation,neurohormonal changes and vascular calcification and stiffness which account for the structural and functional cardiac changes that predispose to excess morbidity and mortality in young people with CKD. 展开更多
关键词 Chronic kidney disease Cardiovascular mortality Cardiorenal syndrome Endothelial dysfunction vascular calcification and stiffness
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