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Matrix metalloproteinases contribute to kidney fibrosis in chronic kidney diseases 被引量:22
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作者 Hong Zhao Yanting Dong +6 位作者 Xinrui Tian Thian Kui Tan Zhuola Liu Ye Zhao Yun Zhang David CH Harris Guoping Zheng 《World Journal of Nephrology》 2013年第3期84-89,共6页
Matrix metalloproteinases(MMPs) are members of the neutral proteinase family. They were previously thought to be anti-fibrotic because of their ability to degrade and remodel of extracellular matrix. However, recent s... Matrix metalloproteinases(MMPs) are members of the neutral proteinase family. They were previously thought to be anti-fibrotic because of their ability to degrade and remodel of extracellular matrix. However, recent studies have shown that MMPs are implicated in initiation and progression of kidney fibrosis through tubular cell epithelial–mesenchymal transition(EMT) as well as activation of resident fibroblasts, endothelial-mesenchymal transition(Endo MT) and pericyte-myofibroblast transdifferentiation. Interstitial macrophage infiltration has also been shown to correlate with the severity of kidney fibrosis in various chronic kidney diseases. MMPs secreted by macrophages, especially MMP-9, hasbeen shown by us to be profibrotic by induction of tubular cells EMT. EMT is mainly induced by transforming growth factor-β(TGF-β). However, MMP-9 was found by us and others to be up-regulated by TGF-β1 in kidney tubular epithelial cells and secreted by activated macrophages, resulting in EMT and ultimately kidney fibrosis. Therefore, MMP-9 may serve as a potential therapeutic target to prevent kidney fibrosis in chronic kidney disease. This review, by a particular focus on EMT, seeks to provide a comprehensive understanding of MMPs, especially MMP-9, in kidney fibrosis. 展开更多
关键词 Matrix metalloproteinase Chronic kidney disease kidney fibrosis Epithelial–mesenchymal transition Transforming growth factor-β
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ELABELA-derived peptide ELA13 attenuates kidney fibrosis by inhibiting the Smad and ERK signaling pathways
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作者 Zhibin YAN Ying SHI +2 位作者 Runling YANG Jijun XUE Caiyun FU 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2024年第4期341-353,共13页
Kidney fibrosis is an inevitable result of various chronic kidney diseases(CKDs)and significantly contributes to end-stage renal failure.Currently,there is no specific treatment available for renal fibrosis.ELA13(amin... Kidney fibrosis is an inevitable result of various chronic kidney diseases(CKDs)and significantly contributes to end-stage renal failure.Currently,there is no specific treatment available for renal fibrosis.ELA13(amino acid sequence:RRCMPLHSRVPFP)is a conserved region of ELABELA in all vertebrates;however,its biological activity has been very little studied.In the present study,we evaluated the therapeutic effect of ELA13 on transforming growth factor-β1(TGF-β1)-treated NRK-52E cells and unilateral ureteral occlusion(UUO)mice.Our results demonstrated that ELA13 could improve renal function by reducing creatinine and urea nitrogen content in serum,and reduce the expression of fibrosis biomarkers confirmed by Masson staining,immunohistochemistry,real-time polymerase chain reaction(RT-PCR),and western blot.Inflammation biomarkers were increased after UUO and decreased by administration of ELA13.Furthermore,we found that the levels of essential molecules in the mothers against decapentaplegic(Smad)and extracellular signal-regulated kinase(ERK)pathways were reduced by ELA13 treatment in vivo and in vitro.In conclusion,ELA13 protected against kidney fibrosis through inhibiting the Smad and ERK signaling pathways and could thus be a promising candidate for anti-renal fibrosis treatment. 展开更多
关键词 ELA13 kidney fibrosis INFLAMMATION SMAD Extracllular signal-regulated kinase(ERK)
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Progress in drug delivery system for fibrosis therapy 被引量:2
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作者 Lei Xing Xin Chang +5 位作者 Lijun Shen Chenglu Zhang Yatong Fan Chongsu Cho Zhiqi Zhang Hulin Jiang 《Asian Journal of Pharmaceutical Sciences》 SCIE CAS 2021年第1期47-61,共15页
Fibrosis is a necessary process in the progression of chronic disease to cirrhosis or even cancer,which is a serious disease threatening human health.Recent studies have shown that the early treatment of fibrosis is t... Fibrosis is a necessary process in the progression of chronic disease to cirrhosis or even cancer,which is a serious disease threatening human health.Recent studies have shown that the early treatment of fibrosis is turning point and particularly important.Therefore,how to reverse fibrosis has become the focus and research hotspot in recent years.So far,the considerable progress has been made in the development of effective anti-fibrosis drugs and targeted drug delivery.Moreover,the existing research results will lay the foundation for more breakthrough delivery systems to achieve better anti-fibrosis effects.Herein,this review summaries anti-fibrosis delivery systems focused on three major organ fibrotic diseases such as liver,pulmonary,and renal fibrosis accompanied by the elaboration of relevant pathological mechanisms,which will provide inspiration and guidance for the design of fibrosis drugs and therapeutic systems in the future. 展开更多
关键词 Fibrotic disease Liver fibrosis Lung fibrosis kidney fibrosis ANTI-fibrosis Drug delivery system
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Design and discovery of a highly potent ultralong-acting GLP-1 and glucagon co-agonist for attenuating renal fibrosis
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作者 Qian Zhao Jiale Dong +14 位作者 Han Liu Hui Chen Huan Yu Shuyin Ye Shuangjin Yu Yu Li Longhui Qiu Nazi Song Hongjiao Xu Qi Liu Zhiteng Luo Yuyi Li Rui Wang Guodong Chen Xianxing Jiang 《Acta Pharmaceutica Sinica B》 SCIE CAS CSCD 2024年第3期1283-1301,共19页
The role of co-agonists of glucagon-like peptide-1 receptor(GLP-1R)and glucagon receptor(GCGR)in chronic kidney disease(CKD)remains unclear.Herein we found that GLP-1R and GCGR expression levels were lower in the kidn... The role of co-agonists of glucagon-like peptide-1 receptor(GLP-1R)and glucagon receptor(GCGR)in chronic kidney disease(CKD)remains unclear.Herein we found that GLP-1R and GCGR expression levels were lower in the kidneys of mice with CKD compared to healthy mice and were correlated with disease severity.Interestingly,GLP-1R or GCGR knockdown aggravated the progression of kidney injury in both diabetic db/db mice and non-diabetic mice undergoing unilateral ureteral obstruction(UUO).Based on the importance of GLP-1R and GCGR in CKD,we reported a novel monomeric peptide,1907-B,with dual-agonism on both GLP-1R and GCGR.The data confirmed that 1907-B had a longer half-life than long-acting semaglutide in rats or cynomolgus monkeys(~2-3 fold)and exhibited better therapeutic contribution to CKD than best-in-class monoagonists,semaglutide,or glucagon,in db/db mice and UUO mice.Various lock-of-function models,including selective pharmacological activation and genetic knockdown,confirmed that 1907-B’s effects on ameliorating diabetic nephropathy in db/db mice,as well as inhibiting kidney fibrosis in UUO mice,were mediated through GLP-1 and glucagon signaling.These findings highlight that 1907-B,a novel GLP-1R and GCGR co-agonist,exerts multifactorial improvement in kidney injuries and is an effective and promising therapeutic option for CKD treatment. 展开更多
关键词 GLP-1 receptor Glucagon receptor Chronic kidney disease Diabetic nephropathy kidney fibrosis Dual-agonism
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Could mycophenolate mofetil combined with benazapril delay tubulointerstitial fibrosis in 5/6 nephrectomized rats? 被引量:4
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作者 LIU Wen-hu TANG Ni-na ZHANG Qi-dong 《Chinese Medical Journal》 SCIE CAS CSCD 2009年第2期199-204,共6页
Background It was reported that combination of mycophenolate mofetil (MMF) and enalapril could reduce proteinuria, improve renal function, and down-regulate diabetes-induced macrophage recruitment and expression of ... Background It was reported that combination of mycophenolate mofetil (MMF) and enalapril could reduce proteinuria, improve renal function, and down-regulate diabetes-induced macrophage recruitment and expression of monocyte chemotactic protein 1 (MCP-1) and transforming growth factor 13 (TGF-13) in diabetic renal tissue. But there are no compelling data available for the combination of MMF and angiotensin converting enzyme inhibitor (ACEI) for suppressing tubulointerstitial fibrosis in chronic kidney diseases. The present study was to disclose the effect of MMF combined with benazapril on delaying tubulointerstitial fibrosis and its possible mechanisms in 5/6 nephrectomized rats. Methods Fifty male SD rats underwent 5/6 nephrectomy (5/6 NX) were randomized into the following groups: NX (5/6 nephrectomized rats, distilled water, n=10), MMF (MMF 20 mg.kgl.d1, p.o., n=10), Ben (benazepril 10 mg.kg4.d4, p.o., n=10), MMF/Ben (MMF 20 mg.kg4.d4, p.o., and benazapril 10 mg-kg~.d4, p.o., n=-10). They were monitored for proteinuria and systolic blood pressure every two weeks. After 8 weeks of treatment, serum creatinine and blood urea nitrogen were assayed and pathological damage to the kidney were evaluated. Renal expression and serum levels of platelet-derived growth factor-BB (PDGF-BB), matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of metaloproteinase-1 (TIMP-1) were detected by immunohistochemistry and ELISA methods. Results After 8 weeks of treatment, 24-hour proteinuria, serum creatinine and blood urea nitrogen were significantly lower in treated groups compared with the untreated rats. MMF and benazepril combination therapy had a greater effect than either drug alone. MMF alone had no effect on systolic blood pressure, but benazapril and MMF/benazapril could significantly reduce blood pressure. Rats that underwent 5/6 nephrectomy had greater tubulointerstitial inflammatory cell infiltration and collagen accumulation than sham-operated rats; all treatments, especially MMF/benazepril, ameliorated these effects. Tubules in 5/6 nephrectomized rats expressed higher levels of PDGF-BB and TIMP-1 and lower MMP-9 compared with sham-operated rats. MMF and benazepril similarly reversed these phenomenons and combination therapy almost completely restored the expression of these cytokines in renal tissue and their plasma concentration. Conclusions MMF, especially combined with benazepril, can reduce proteinuria, improve renal function, ameliorate tubulointerstitial fibrosis in 5/6 nephrectomized rats. These effects might be, in part, associated with down-regulation of PDGF-BB and TIMP-1,End MMP-9 up-regulation in renal tissues. Chin Med J 2009; 122(2): 199-204 展开更多
关键词 kidney fibrosis angiotensin-converting enzyme inhibitors
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Effect of Yishen Huayu Fang on kidney tissue E-cadherin expression in unilateral ureter ligation in rats 被引量:6
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作者 张琳琪 李伟明 孙伟 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2012年第2期273-277,共5页
OBJECTIVE:To observe E-calcium sticky protein(E-cadherin) expression in kidney tissues in a rat model of unilateral ureter ligation and the effect of Yishen Huayu Fang(formula of tonifying the kidney and dissolving ac... OBJECTIVE:To observe E-calcium sticky protein(E-cadherin) expression in kidney tissues in a rat model of unilateral ureter ligation and the effect of Yishen Huayu Fang(formula of tonifying the kidney and dissolving accumulated blood stasis) on the expression.METHODS:A total of 150 clean grade male rats were randomly divided into a control group,model group,low-dose Yishen Huayu Fang group(low-dose group),high-dose Yishen Huayu Fang group(high-dose group),and Lotensin group.A renal fibrosis model was established with unilateral ureteral obstruction(UUO).Pathological changes of rat renal tissue were observed with light microscopy on days 3,7,14,21,and 28 after UUO.Changes in kidney tissue E-cadherin expression were observed with immunohistochemistry.RESULTS:Three days after modeling,kidney edema appeared followed by gradual inflammatory cell infiltration,and part of the small tubules disappeared while the renal cortex thinned.Meanwhile,the E-cadherin expression level dropped,which was negatively correlated with the obstruction time.After intervention,E-cadherin expression was increased in all treatment groups(P<0.01 or P<0.05),while there were no significant differences between the high-dose and Lotensin groups.CONCLUSION:Yishen Huayu Fang delays the renal fibrosis process by promoting E-cadherin expression in renal tissues and reducing extracellular matrix deposition. 展开更多
关键词 Yishen Huayu Fang Formula of tonifying the kidney and dissolving accumulated blood stasis Renal fibrosis Unilateral ureter ligation E-calcium mucin
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