Effects of Yerba Mate Consumption (Ilex paraguariensis) on Cardiac Remodeling in Rats

This study investigated the effects of yerba mate consumption, a South American beverage, on cardiac remodeling in rats. For this purpose, 24 male Wistar rats were divided into Control Group (CG) which received filtered water and a standard diet, and Yerba Mate Group (YM), 6 g of Ilex paraguariensis in 100 ml water and the same diet, for 30 days. The YM group showed a reduction in final body weight and food consumption without altering weight gain. Regarding cardiac remodeling, the YM group exhibited a decrease in the right ventricle weight/final body weight ratio, suggesting cardiac atrophy, without affecting the atria and left ventricle. There was no change in cardiomyocyte area or nuclear fractal dimension in both groups. However, animals that consumed yerba mate showed increased collagen deposition and a smaller fractal dimension in the left ventricle. The consumption of yerba mate at room temperature for 30 days induced changes in cardiac remodeling, as evidenced by increased collagen deposition and alterations in fractal dimension in the left ventricle.

Evidence-Based Complementary and Alternative Medicine Effects of Capybara Oil on Cardiac Remodeling of C57bl/6 Mice

Cardiovascular diseases are the main cause of morbidity and mortality in the world, and obesity and the metabolic syndrome are risk factors for its development. One of the therapies to reduce cardiovascular risk is the use of polyunsaturated fatty acids. In Brazil, a source of such acid is the oil extracted from the fat of the capybara. The objective of this work is to study the effects of the capybara oil on lipid and glucose metabolism, as well as its effects on the adipose tissue and cardiac remodeling. We assessed the effects of capybara oil treatment on body mass, lipid and carbohydrate metabolism, systolic blood pressure, adipose tissue and cardiac remodeling, and performed an ultrastructural evaluation of the myocardium in C57Bl/6 mice treated with high-fat diet. Treatment with capybara oil reduced total cholesterol and triglyceride levels, systolic blood pressure, visceral and subcutaneous adipose tissue, and adipocyte diameter. In addition, cardiac remodeling was attenuated, preserving cardiomyocytes, increasing vascularization, reducing cardiomyocyte hypertrophy and the extracellular matrix, and preserving the morphological integrity of mitochondria. Capybara oil has several beneficial effects on the cardiovascular and metabolic system, and further studies are needed to better understand its role in the prevention or treatment of cardiovascular diseases.

AMPK and cardiac remodelling

Cardiac remodelling is generally accepted as a critical process in the progression of heart failure. Myocyte hypertrophy,inflammatory responses and cardiac fibrosis are the main pathological changes associated with cardiac remodelling.AMP-activated protein kinase(AMPK) is known as an energy sensor and a regulator of cardiac metabolism under normal and ischaemic conditions. Additionally, AMPK has been shown to play roles in cardiac remodelling extending well beyond metabolic regulation. In this review, we discuss the currently defined roles of AMPK in cardiac remodelling and summarize the effects of AMPK on cardiac hypertrophy, inflammatory responses and fibrosis and the molecular mechanisms underlying these effects. In addition, we discuss some pharmacological activators of AMPK that are promising treatments for cardiac remodelling.

Pyroptosis is a drug target for prevention of adverse cardiac remodeling: The crosstalk between pyroptosis, apoptosis, and autophagy

Acute myocardial infarction(AMI)is one of the main reasons of cardiovascular disease-related death.The introduction of percutaneous coronary intervention to clinical practice dramatically decreased the mortality rate in AMI.Adverse cardiac remodeling is a serious problem in cardiology.An increase in the effectiveness of AMI treatment and prevention of adverse cardiac remodeling is difficult to achieve without understanding the mechanisms of reperfusion cardiac injury and cardiac remodeling.Inhibition of pyroptosis prevents the development of postinfarction and pressure overload-induced cardiac remodeling,and mitigates cardiomyopathy induced by diabetes and metabolic syndrome.Therefore,it is reasonable to hypothesize that the pyroptosis inhibitors may find a role in clinical practice for treatment of AMI and prevention of cardiac remodeling,diabetes and metabolic syndrome-triggered cardiomyopathy.It was demonstrated that pyroptosis interacts closely with apoptosis and autophagy.Pyroptosis could be inhibited by nucleotide-binding oligomerization domain-like receptor with a pyrin domain 3 inhibitors,caspase-1 inhibitors,microRNA,angiotensin-converting enzyme inhibitors,angiotensinⅡreceptor blockers,and traditional Chinese herbal medicines.

Protective effects of rice bran hydrolysates on heart rate variability,cardiac oxidative stress,and cardiac remodeling in high fat and high fructose diet-fed rats

Objective:To examine the ameliorative effect of rice bran hydrolysates(RBH)on metabolic disorders,cardiac oxidative stress,heart rate variability(HRV),and cardiac structural changes in high fat and high fructose(HFHF)-fed rats.Methods:Male Sprague-Dawley rats were daily fed either standard chow diet with tap water or an HFHF diet with 10%fructose in drinking water over 16 weeks.RBH(500 and 1000 mg/kg/day)was orally administered to the HFHF-diet-fed rats during the last 6 weeks of the study period.At the end of the treatment,metabolic parameters,oxidative stress,HRV,and cardiac structural changes were examined.Results:RBH administration significantly ameliorated metabolic disorders by improving lipid profiles,insulin sensitivity,and hemodynamic parameters.Moreover,RBH restored HRV,as evidenced by decreasing the ratio of low-frequency to highfrequency power of HRV,a marker of autonomic imbalance.Cardiac oxidative stress was also mitigated after RBH supplementation by decreasing cardiac malondialdehyde and protein carbonyl,upregulating eNOS expression,and increasing catalase activity in the heart.Furthermore,RBH mitigated cardiac structural changes by reducing cardiac hypertrophy and myocardial fibrosis in HFHFdiet-fed rats.Conclusions:The present findings suggest that consumption of RBH may exert cardioprotective effects against autonomic imbalances,cardiac oxidative stress,and structural changes in metabolic syndrome.

Modification of Serum Galectin-3 and Reversal of Cardiac Remodeling Following Pediatric Transcatheter Atrial Septal Defect Closure

Objectives:We aimed to evaluate the effect of percutaneous atrial septal defect(ASD)closure in children using right heart indices and serum galectin-3(Gal-3),as potential biomarkers of right heart remodeling.Methods:This case–control prospective study included 40 children with ASD and 25 control subjects.An echocardiographic evaluation was performed before the procedure,as well as 24 h,1 month,and 6 months after intervention.Serum Gal-3 was measured before,and 1 month after the procedure.Results:Serum Gal-3 concentration,right atrial(RA)dimensions,right ventricular(RV)dimensions,indexed RA area,and right index of myocardial performance(RIMP)were significantly increased in children with ASD compared with control subjects while tricuspid annular plane systolic excursion(TAPSE)was significantly decreased.Six months after closure,RA,and RV dimensions significantly decreased and RVfunction improved(RIMP decreased and TAPSE increased).Gal-3 oncentration significantly decreased 1 month after ASD closure,but it did not reach normal range compared with control subjects.A positive correlation between Gal-3 and age at closure,RA area,RV dimensions,and RIMP was observed.A positive correlation was observed between the decrease in Gal-3 concentration and the decrease in RA area and RV dimensions 1 month after ASD closure.A significant negative correlation was observed between TAPSE and Gal-3 concentration before and after intervention.Conclusions:Percutaneous ASD closure can improve right-sided indices and decrease serum Gal-3 concentration.Gal-3 can be used as a sensitive biomarker of right heart remodeling,with a decrease in Gal-3 concentration suggesting reversal of maladaptive remodeling.

Sphingosine-1-Phosphate Protects Against the Development of Cardiac Remodeling via Sphingosine Kinase 2 and the S1PR2/ERK Pathway

Objective:Cardiac remodeling is a common pathological change in various cardiovascular diseases and can ultimately result in heart failure.Thus,there is an urgent need for more effective strategies to aid in cardiac protection.Our previous work found that sphingosine-1-phosphate(S1P)could ameliorate cardiac hypertrophy.In this study,we aimed to investigate whether S1P could prevent cardiac fibrosis and the associated mechanisms in cardiac remodeling.Methods:Eight-week-old male C57BL/6 mice were randomly divided into a sham,transverse aortic constriction(TAC)or a TAC+S1P treatment group.Results:We found that S1P treatment improved cardiac function in TAC mice and that the cardiac fibrosis ratio in the TAC+S1P group was significantly lower and was accompanied by a decrease inα-smooth muscle actin(α-SMA)and collagen type I(COL I)expression compared with the TAC group.We also found that one of the key S1P enzymes,sphingosine kinase 2(SphK2),which was mainly distributed in cytoblasts,was downregulated in the cardiac remodeling case and recovered after S1P treatment in vivo and in vitro.In addition,our in vitro results showed that S1P treatment activated extracellular regulated protein kinases(ERK)phosphorylation mainly through the S1P receptor 2(S1PR2)and spurred p-ERK transposition from the cytoplasm to cytoblast in H9c2 cells exposed to phenylephrine.Conclusion:These findings suggest that SphK2 and the S1PR2/ERK pathway may participate in the anti-remodeling effect of S1P on the heart.This work therefore uncovers a novel potential therapy for the prevention of cardiac remodeling.

Cardiac stromal cells on stage:From dull filler to specialized actors

Cardiac stromal cells have faced through the years a significant evolution in their definitions concerning their phenotypes,markers,and functions.They are surging to key roles in physiopathology,becoming important targets to be exploited for cardiac repair.In this perspective,we briefly discuss their role in novel therapeutic strategies for enhancing cardiac repair and regeneration.

Ameliorative Influence of Dietary Dates on Doxorubicin-Induced Cardiac Toxicity

Doxorubicin is a commonly used anticancer agent, which may cause cardiac toxicity. The present study designed to evaluate Phoenix dactylofera (dates) in doxorubicin (DXR) induced cardiac toxicity and cardiac remodeling in Wistar albino rats. The experimental rats procured, acclimatized and finally divided into five groups (n = 6). Group I served as normal controls, group II served as disease controls and groups 3, 4 & 5 served as therapeutic groups (Phoenix dactylofera 5%, 10%, and 15% respectively). Cardiac remodeling and toxicity in the rats were induced by administration of DXR (1.25 mg/kg i.p. in 16 divided doses/month). At the end of protocol, effect of Phoenix dactylofera on cardiac remodeling was evaluated by measuring parameters like haemodynamics, heart weight, anatomy, Troponin T, creatine phosphokinase (CPK), creatine phosphokinase-MB (CPK-MB), Lactate dehydrogenase (LDH), serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), calcium ion Ca2+, sodium ion Na+, potassium ion K+, intracellular enzymes like Malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT). The disease control groups showed significantly elevated (p dactylofera significantly (p 2+, Na+, K+ levels to a normal value. Further, the histological studies of the cardiac tissues demonstrated that the normal architecture of the cardiac cells was restored in the animals fed with dietary Phoenix dactylofera as compared to disease controls. The findings show that the administration of Phoenix dactylofera has the potential to prevent the toxicity induced by doxorubicin in the experimental rats.

Effect of Different Styles of Coronary Heart Disease and Its Risk Factors on Cardiac Remodeling and Dysfunction

Objectives To evaluate the effect of different styles of coronary heart disease （CHD）, different regions of acute myocardial infarction （AMI）, its risk factors and branches of coronary stenosis on left ventricular remodeling and dysfunction by applying echocardiography. Methods 251 patients with CHD and 96 patients without CHD （NoCHD） were verified by selective coronary angiography. CHD patients were divided into stable angina pectoris （SAP） 26, unstable angina pectoris（UAP） 53, acute myocardial infarction （AMI） 140 and old myocardial infarction （OMI） 30 based on clinical situation, cTnT, cardiac enzyme and ECG. AMI patients were further divided into subgroups including acute anterior myocardial infarct （Aa,n = 53）, acute inferior myocardial infarction （Ai, n=54） and Aa＋Ai （n=33） based on ECG. Cardiac parameters： end-diastolic interventricular septum thickness（IVSd）, end-diastolic left ventricular internal diameter （LVd）, left ventricular mass （LM）, end-diastolic left ventricular volume （EDV）, end-systolic left ventricular volume （ESV） and left ventricular ejection fraction（LVEF） were measured by ACUSON 128XP/10 echocardiography. Multiples linear regression analyses were performed to test statistical associations between LVEF and the involved branches of coronary stenosis, blood pressure, lipids, glucose and etc after onset of myocardial infarction. Results EDV and ESV were increased and LVEF decreased on patients with AMI,OMI and UAP （P〈0.05-0.0001）. LM was mainly increased in patients with OMI （P〈0.01） and LVd was mainly enlarged in patients with AMI. EF was significantly decreased and EDV, ESV, LM and LVd were remarkably increased in AMI patients with Aa and Aa＋Ai. With the multiple linear regression analyses by SPSS software, we found that LVEF was negatively correlated to the involved branches of coronary stenosis as well as to systolic blood pressure after onset of myocardial infarction while there was no significant correlation between LVEF and other factors. LVEF was significantly decreased, and LVd and LM increased in AMI patients with antecedent hypertension, compared to patients without hypertension （P〈0.001）. Conclusions Effects of different styles of CHD and different regions of AMI on left ventricular remodeling and cardiac function are different. Myocardial infarction, especially Aa and Aa＋Ai, is one of the most important causes of left ventricular remodeling and cardiac dysfunction. Multiple vessel stenosis and systolic blood pressure at the onset of myocardial infarction reduce LVEF in AMI patients. Antecedent hypertension may accelerate the effect of AMI on cardiac remodeling and dysfunction. Therefore primary and secondary preventions of CHD are critical for protecting heart from remodeling and dysfunction.

Mitophagy deficiency activates stimulator of interferon genes activation and aggravates pathogenetic cardiac remodeling

Stimulator of interferon genes(STING)has recentlybeen found to play a crucial role in cardiac sterile inflammation and dysfunction.The role of stimulator of interferon genes(STING)in cardiac sterile inflammation and dysfunction has been recently discovered.This study aims to examine the involvement of STING in pathological cardiac remodeling and the mechanisms that govern the activation of the STING pathway.To investigate this,transverse aortic constriction(TAC)was performed on STING knockout mice to induce pressure over-load-induced cardiac remodeling.Subsequently,cardiac function,remodeling,and inflammation levels were evaluated.The STING pathway was found to be activated in the pressure overload-stressed heart and angiotensin II(Ang Il)-stimulated cardiac fibroblasts.Loss of STING expression led to a significant reduction in inflammatory responses,mitochondrial fragmenta-tion,and oxidative stress in the heart,resulting in attenuated cardiac remodeling and dysfunc-tion.Furthermore,the exacerbation of pressure overload-induced sTING-mediated inflammation and pathological cardiac remodeling was observed when mitophagy was sup-pressed through the silencing of Parkin,an E3 ubiquitin ligase.Taken together,these findings indicate that STING represents a newly identified and significant molecule implicated in the process of pathological cardiac remodeling and that mitophagy is an upstream mechanism that regulates STING activation.Targeting STING may therefore provide a novel therapeutic strategy for pathological cardiac remodeling and heart failure.

Aerobic interval training preconditioning protocols inhibit isoproterenol-induced pathological cardiac remodeling in rats:Implications on oxidative balance,autophagy,and apoptosis

This study aimed to investigate the potential cardioprotective effects of moderate and high-intensity aerobic interval training(MIIT and HIIT)preconditioning.The focus was on histological changes,pro-oxidant-antioxidant balance,autophagy initiation,and apoptosis in myocardial tissue incited by isoproterenol-induced pathological cardiac remodeling(ISO-induced PCR).Male Wistar rats were randomly divided into control(n=6),ISO(n=8),MIIT(n=4),HIIT(n=4),MIIT+ISO(n=8),and HIIT+ISO(n=8)groups.The MIIT and HIIT protocols were administered for 10 weeks,followed by the induction of cardiac remodeling using subcutaneous injection of ISO(100 mg/kg for two consecutive days).Alterations in heart rate(HR),mean arterial pressure(MAP),rate pressure product(RPP),myocardial oxygen consumption(MVO_(2)),cardiac hypertrophy,histopathological changes,prooxidant-antioxidant balance,autophagy biomarkers(Beclin-1,Atg7,p62,LC3Ⅰ/Ⅱ),and apoptotic cell distribution were measured.The findings revealed that the MIIT+ISO and HIIT+ISO groups demonstrated diminished myocardial damage,hemorrhage,immune cell infiltration,edema,necrosis,and apoptosis compared to ISO induced rats.MIIT and HIIT preconditioning mitigated HR,enhanced MAP,and preserved MVO_(2)and RPP.The pro-oxidant-antioxidant balance was sustained in both MIIT+ISO and HIIT+ISO groups,with MIIT primarily inhibiting pro-apoptotic autophagy progression through maintaining pro-oxidant-antioxidant balance,and HIIT promoting pro-survival autophagy.The results demonstrated the beneficial effects of both MIIT and HIIT as AITs preconditioning in ameliorating ISO-induced PCR by improving exercise capacity,hemodynamic parameters,and histopathological changes.Some of these protective effects can be attributed to the modulation of cardiac apoptosis,autophagy,and oxidative stress.

Taurine Inhibits Myocardial Fibrosis via PKC-ERK1/2 Signaling Pathways

Previous studies have demonstrated the important role of taurine in inhibiting proliferation of myofibrob lasts（myoFb） and myocardial fibrosis. However, the underlying mechanisms are unclear. The present study was de signed to shed light on this issue through exploring the signal pathways via in vitro experiments. Angiotension II （AngII） treatment significantly increased myoFb proliferation and the levels of collagens I and III（P〈0.05）, whereas taurine, PKCα（PKC： protein kinase C） specific inhibitor L-threo-dihydro-sphingosine（D4681）, ERK1/2 inhibitor （PD98095） abrogated myoFb proliferation and collagen levels（P〈0.05, P〈0.01, respectively）, and increased the G0/G1 phase rate and decreased S phase rate. Immunocytochemistry, confocal fluorescence staining and image analy sis showed that taurine could inhibit the translocation and expression of p-PKCαin membrane, and then inhibit nuc lear translocation and expression of p-ERK1/2. These results have statistically significant differences compared with those of AngII group（P〈0.01）. Western blot results also show that taurine could inhibit the protein expression of p-PKCα and p-ERK1/2. We used p-PKCα specific inhibitor D4681 in order to elucidate the relationship between p-PKCα and p-ERK1/2 in signal transduction pathways. Finally, the results show that the protein expression of p-ERK1/2 and nuclear translocation were suppressed in D4681 group.

New insights into the cardio-renal benefits of SGLT2 inhibitors and the coordinated role of miR-30 family

Sodium-glucose co-transporter inhibitors(SGLTis)are the latest class of anti-hyper-glycemic agents.In addition to inhibiting the absorption of glucose by the kidney causing glycosuria,these drugs also demonstrate cardio-renal benefits in diabetic subjects.miR-30 family,one of the most abundant microRNAs in the heart,has recently been linked to a setting of cardiovascular diseases and has been proposed as novel biomarkers in kidney dysfunctions as well;their expression is consistently dysregulated in a variety of cardio-renal dysfunctions.The mechanistic involvement and the potential interplay between miR-30 and SGLT2i effects have yet to be thoroughly elucidated.Recent research has stressed the relevance of this clus-ter of microRNAs as modulators of several pathological processes in the heart and kidneys,raising the possibility of these small ncRNAs playing a central role in various cardiovascular complications,notably,endothelial dysfunction and pathological remodeling.Here,we review current evidence supporting the pleiotropic effects of SGLT2is in cardiovascular and renal out-comes and investigate the link and the coordinated implication of the miR-30 family in endo-thelial dysfunction and cardiac remodeling.We also discuss the emerging role of circulating miR-30 as non-invasive biomarkers and attractive therapeutic targets for cardiovascular dis-eases and kidney diseases.Clinical evidence,as well as metabolic,cellular,and molecular as-pects,arecomprehensively covered.

Role of voltage-gated potassium channel α subunits in cardiovascular system

Voltage-gated ion channels(VGICs) are central to cellular excitation, orchestrating skeletal and cardiac muscle contractions and enabling neural signal transduction. Among these, voltage-gated potassium(Kv) channels are particularly significant in cardiac electrophysiology, especially during the repolarization phase of the cardiac action potential. In cardiac myocytes, Kv channels are integral to a multitude of sophisticated functions, including electrical conduction. Despite their importance, research on Kv channels in the context of cardiovascular diseases is limited. This review offers a comprehensive summary of the structural complexities of Kv channels, delineating the regulatory mechanisms involved in channel gating, expression, and membrane localization. Additionally, we examine the role of different Kv α-subunits in modulating Kv channels and their impact on cardiac remodeling, and assess the potential of targeting Kv channels for the development of anti-arrhythmic therapies.

Tenascin-x facilitates myocardial fibrosis and cardiac remodeling through transforming growth factor-β1 and peroxisome proliferator-activated receptor γ in alcoholic cardiomyopathy

Background Tenascin-x, an extracellular matrix glycoprotein exclusively expressed in fibroblasts, can mediate fibrosis in the presence of collagen. Therefore, we have investigated its potential role in facilitating myocardial fibrosis and cardiac remodeling via the transforming growth factor-lβ1 and peroxisome proliferator-activated receptor γ（TGFβ1-PPARγ） pathway in alcoholic cardiomyopathy （ACM）.Methods Experimental animals were divided into control （group A） and tenascin-x knock-out groups （group B）receiving alcohol. Six months post treatment, cardiac ejections fraction （EF）, fractional shortening （FS）, left ventricle end-diastole internal diameter （LVEDd） and collagen column fraction （CVF） were observed. Tenascin-x, smad-3, TGFβ1,smad-7 and PPARγ protein expression levels were detected by Western blotting.Results Six months post treatment, EF and FS values were higher in group B than in group A （P 〈0.05 and P 〈0.01,respectively）, while LVEDd and CVF were lower in group B （P 〈0.05 and P 〈0.01, respectively）. Tenascin-x, smad-3 and TGFβ1 protein expression levels were higher in group A, while smad-7 and PPARY levels were lower than in group B （P〈0.01）, as measured by immunohistochemistry and Western blotting. Tenascin-x protein expression was negatively correlated with EF, FS, smad-7 and PPARγ, and positively correlated with LVEDd, CVF, smad-3, and TGFβ1 （P 〈0.001）.Conclusion Tenascin-x is an initiator of myocardial fibrosis and ACM development via upregulation of TGFβ1 and downregulation of PPARγ.

Lipopolysaccharide induced activin A-follistatin imbalance affects cardiac fibrosis

Background Inflammation plays a pivotal role in cardiac remodeling, especially in myocardial fibrosis. Abnormal growth of cardiac fibroblasts is critically involved in the pathophysiology of cardiac hypertrophy/remodeling. Previous study has demonstrated that many inflammation stimulating factors trigger transforming growth factor-β （TGF-β） induction and reactive myocardial fibrosis. Activin A （ACT A） is a member of TGF-β superfamily, and follistatin （FS） is an activin-binding protein, i.e. an antagonist of ACT A. Our previous studies have shown that ACT A-FS imbalance occurs in rats with heart failure （HF）, and overexpression of ACT A can lead to ventricular remodeling, and resultant HF. Low expression of FS after myocardial infarction further exacerbated HF. The pathogenic change resulting from overexpression of ACT A is consistent with that of overexpression of angiotensin II （Angll）. Ventricular remodeling includes cardiocyte remodeling and myocardial interstitial collagen deposition and fibrosis, Therefore, the present study was designed to investigate the effects of inflammatory factors on the ACT A-FS and the secretions of cardiac fibroblasts in order to explore in depth the mechanism of myocardial fibrosis. Methods A rat model with HF was established, and the results showed that there was a greater degree of cardiac fibrosis in HF rats. In addition, we found that there was an imbalance of the ACT A/FS system in HF rats, which was characterized by increased levels of ACT A. Further, primary rat cardiac fibroblasts were cultured and the MTT assay was performed to determine the effect of the inflammatory factor-bacterial endotoxin lipopolysaccharide （LPS） on cardiac fibroblast proliferation. Results The results showed that LPS can stimulate the cardiac fibroblasts to proliferate in a dose-dependent manner. Cellular immunohistochemical staining showed that the rat cardiac fibroblasts themselves could express ACT A and FS proteins, and stimulation by LPS could apparently promote the cultured primary rat cardiac fibroblasts to secrete ACT A, but inhibit the secretion of FS. The results also showed that ACT A promoted, in a dose-dependent manner, the proliferation of the cultured primary rat cardiac fibroblasts, and the expression of collagen types I and Ill. Moreover, ACT A promoted, in a dose dependent manner, the cardiac fibroblasts to secrete nitric oxide （NO）, and unregulated the expression of inducible nitric oxide synthase （iNOS） mRNA. Conclusions These results suggest that the inflammatory mediator LPS can promote ACT A-FS imbalance in cardiac fibroblasts, mainly overexpression of ACT A. Overexpression of ACT A promotes the proliferation and the secretion of collagens in cardiac fibroblasts through autocrine/paracrine stimulation of NO, and is involved in the pathological process of myocardial fibrosis.

microRNAs in cardiac regeneration and cardiovascular disease

microRNAs(miRNAs)are a class of small non-coding RNAs,which have been shown important to a wide range of biological process by post-transcriptionally regulating the expression of protein-coding genes.miRNAs have been demonstrated essential to normal cardiac development and function.Recently,numerous studies indicate miRNAs are involved in cardiac regeneration and cardiac disease,including cardiac hypertrophy,myocardial infarction and cardiac arrhythmia.These observations suggest miRNAs play important roles in cardiology.In this review,we summarize the recent progress of studying miRNAs in cardiac regeneration and cardiac disease.We also discuss the diagnostic and therapeutic potential of miRNAs in heart disease.

Growth factors induce the improved cardiac remodeling in autologous mesenchymal stem cell-implanted failing rat hearts

Therapeutically delivered mesenchymal stem cells (MSCs) improve ventricular remodeling. However,the mechanism underlying MSC cardiac remodeling has not been clearly determined. Congestive heart failure (CHF) was induced in rats by cauterization of the left ventricular free wall. MSCs were cultured from autologous bone marrow and injected into the border zone and the remote myocardium 5 d after injury. Ten weeks later,when compared with sham operation,CHF significantly increased nucleus mitotic index,capillary density,and expression of insulin-like growth factor 1,hepatocyte growth factor and vascular endothelial growth factor in the border zone (P<0.01) and decreased each of them in the remote myocardium (P<0.05 or P<0.01). MSC implantation in CHF dramatically elevated ex-pression of these growth factors in the remote myocardium and further elevated their expression in the border zone when compared with CHF without MSC addition (P<0.05 or P<0.01). This was paralleled by a higher nucleus mitotic index and a significantly increased capillary density both in the remote myocardium and in the border zone,and by a lower percentage of area of collagen and a higher percentage of area of myocardium in the border zone (P<0.05 or P<0.01),and cardiac remodeling markedly improved. Autologous MSC implantation promoted expression of growth factors in rat failing myocardium,which might enhance cardiomyogenesis and angiogenesis,and improved cardiac remodeling.

Effect of Moxibustion on Cardiac Remodeling and Myocardial Function in Rats with Exercise-Induced Fatigue

Objective:To explore the effect of moxibustion at Shenque(CV8)on myocardial structure and function in rats with exercise-induced fatigue.Methods:A 12-week treadmill training program was used to establish a rat model of exercise-induced fatigue.Fifty-six male SD rats removed six rats that did not reach the molding condition,Remaining rats were randomly divided into the following five groups:a normal group(n=10)that did not under go the exercise routine and were not treated,a control group(n=10)that did not under go the exercise routine,but received a mild dose of moxibustion at"Shenque"(CV 8)for 15 min,an untreated group(n=10)that received no treatment after exercise,a CV 8 group(n=10)that received a mild dose of moxibustion at"Shenque"(CV 8)for 15 min after exercise,a non-acupoint(tail)group(n=10)that received a mild dose of moxibustion at"non-acupoint"for 15 min after exercise.At one hour after the end of the 12-week training program,the left ventricular diastolic volume(LVDV),left ventricular systolic volume(LVSV),peak early diastolic mitral blood flow velocity(E),and peak late diastolic mitral blood flow velocity(A)were measured,and the E/A ratio were calculated.The serum myoglobin(Mb),creatine kinase-muscle/brain(CK-MB),and cardiac troponin-I(cTnI)levels were detected using an automatic biochemical analyzer.Results:When the values obtained before and after treatment were compared within the same groups,the LVDV,LVSV,E,and A were increased(P<0.05 or P<0.01),and the E/A were decreased(P<0.01)in the untreated group and the tail group.Regarding inter-group comparisons,the LVDV,LVSV,E,and A were increased(P<0.05 or P<0.01),and the E/A were decreased(P<0.01)in the untreated group and the tail group compared to the normal group and control group.Compared to the untreated group and the tail group,the LVDV,LVSV,E,and A were decreased(P<0.01)and the E/A were increased(P<0.01)in the CV 8 group.Compared to the normal group and the control group,the serum Mb,CK-MB,and cTnI levels were increased(P<0.01)in the untreated group and the tail group,and the serum Mb and CK-MB levels were also increased(P<0.01)in the CV 8 group.Compared to the untreated group and the tail group the serum Mb,CK-MB,and cTnI levels in the CV 8 group were decreased(P<0.01).Conclusions:Moxibustion at Shenque(CV8)can effectively prevent cardiac structural changes caused by exercise-induced fatigue and enhance heart function.This treatment does not have side effects in healthy rats and is a safe and effective technique..