Endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication

Leucker, Thorsten M.; Jones, Steven P.

doi:10.3389/fphys.2014.00328

Cited by 26 publications

(26 citation statements)

References 90 publications

(100 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Previous data indicate that abnormal cross‐talk between endothelial cells and cardiomyocytes plays an important role in the pathogenesis of heart failure (Tirziu et al . ; Leucker & Jones, ) and cardiac hypertrophy (Tirziu & Simons, ). Alternatively, our findings may represent the effect of an endothelium‐specific mechanism including augmented coronary microvascular function in the setting of pressure overload and/or an attenuation of another proposed mechanism underling cardiac fibrosis, such as endothelial to mesenchymal transition (Zeisberg et al .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Augmented endothelial l‐arginine transport ameliorates pressure‐overload‐induced cardiac hypertrophy

Rajapakse

Johnston

Kiriazis

et al. 2015

Experimental Physiology

View full text Add to dashboard Cite

New Findings r What is the central question of this study?What is the potential role of endothelial NO production via overexpression of the l-arginine transporter, CAT1, as a mitigator of cardiac hypertrophy? r What is the main finding and its importance?Augmentation of endothelium-specific l-arginine transport via CAT1 can attenuate pressure-overload-dependent cardiac hypertrophy and fibrosis. Our findings support the conclusion that interventions that improve endothelial l-arginine transport may provide therapeutic utility in the setting of myocardial hypertrophy. Such modifications may be introduced by exercise training or locally delivered gene therapy, but further experimental and clinical studies are required.Endothelial dysfunction has been postulated to play a central role in the development of cardiac hypertrophy, probably as a result of reduced NO bioavailability. We tested the hypothesis that increased endothelial NO production, mediated by increased l-arginine transport, could attenuate pressure-overload-induced cardiac hypertrophy. Echocardiography and blood pressure measurements were performed 15 weeks after transverse aortic constriction (TAC) in wild-type (WT) mice (n = 12) and in mice with endothelium-specific overexpression of the l-arginine transporter, CAT1 (CAT+; n = 12). Transverse aortic constriction induced greater increases in heart weight to body weight ratio in WT (by 47%) than CAT+ mice (by 25%) compared with the respective controls (P ࣘ 0.05). Likewise, the increase in left ventricular wall thickness induced by TAC was significantly attenuated in CAT+ mice (P = 0.05). Cardiac collagen type I mRNA expression was greater in WT mice with TAC (by 22%; P = 0.03), but not in CAT+ mice with TAC, compared with the respective controls. Transverse aortic constriction also induced lesser increases in β-myosin heavy chain mRNA expression in CAT+ mice compared with WT (P ࣘ 0.05). Left ventricular systolic pressure after TAC was 36 and 39% greater in WT and CAT+ mice, respectively, compared with the respective controls (P ࣘ 0.001). Transverse aortic constriction had little effect on left ventricular end-diastolic pressure in both genotypes. Taken together, these data indicate that augmenting endothelial function by overexpression of l-arginine transport can attenuate pressure-overload-induced cardiac hypertrophy.

show abstract

Section: Discussionmentioning

confidence: 99%

“…It is known that normal endothelial function is critical for the regulation of cardiac function and that impaired endothelial function can lead to abnormalities in cardiac contractility, cardiomyocyte proliferation/apoptosis and cardiac hypertrophy (Chin‐Dusting et al . ; Leucker & Jones, ; Mordi & Tzemos, ; McCormick et al . ).…”

Section: Introductionmentioning

confidence: 99%

Augmented endothelial l‐arginine transport ameliorates pressure‐overload‐induced cardiac hypertrophy

Rajapakse

Johnston

Kiriazis

et al. 2015

Experimental Physiology

View full text Add to dashboard Cite

show abstract

“…Endothelial cells are covered by surface proteoglycans that form part of the barrier functions of the blood-tissue interface [128]. Endothelial cells are a main cell type in the vasculature and contribute to the maintenance of vascular tone and cardiac repair [129]. Vascular leaks of fluid from the plasma to the interstitial space contribute to inflammation and myocardial dysfunction.…”

Section: Endothelial Dysfunctionmentioning

confidence: 99%

Novel Insights into the Role of HDL-Associated Sphingosine-1-Phosphate in Cardiometabolic Diseases

Diarte-Añazco

Méndez-Lara

Pérez

et al. 2019

IJMS

View full text Add to dashboard Cite

Sphingolipids are key signaling molecules involved in the regulation of cell physiology. These species are found in tissues and in circulation. Although they only constitute a small fraction in lipid composition of circulating lipoproteins, their concentration in plasma and distribution among plasma lipoproteins appears distorted under adverse cardiometabolic conditions such as diabetes mellitus. Sphingosine-1-phosphate (S1P), one of their main representatives, is involved in regulating cardiomyocyte homeostasis in different models of experimental cardiomyopathy. Cardiomyopathy is a common complication of diabetes mellitus and represents a main risk factor for heart failure. Notably, plasma concentration of S1P, particularly high-density lipoprotein (HDL)-bound S1P, may be decreased in patients with diabetes mellitus, and hence, inversely related to cardiac alterations. Despite this, little attention has been given to the circulating levels of either total S1P or HDL-bound S1P as potential biomarkers of diabetic cardiomyopathy. Thus, this review will focus on the potential role of HDL-bound S1P as a circulating biomarker in the diagnosis of main cardiometabolic complications frequently associated with systemic metabolic syndromes with impaired insulin signaling. Given the bioactive nature of these molecules, we also evaluated its potential of HDL-bound S1P-raising strategies for the treatment of cardiometabolic disease.

show abstract

“…These excessive ROS such as superoxide can react with NO to form peroxynitrite (ONOO − ) [45], thereby reducing the available NO level for proper endothelial function. Thus, high ROS generation may lead to different abnormalities including endothelial dysfunction [46,47]. Findings from this study showed 8-OHdG, a marker for oxidative stress to signi cantly increase with increasing quartiles of ADMA and also positively correlated with ADMA.…”

Section: Discussionmentioning

confidence: 65%

Cardiovascular Risk Factors and their Relationship with Endothelial Dysfunction in Rural and Urban South African Children

Matjuda

Engwa

Anye

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Endothelial dysfunction is known to be an initiator to the development and progression of atherosclerotic cardiovascular disease (CVD). However, there is paucity o knowledge on its relationship with cardiovascular risk factors in children. More so, some of these cardiovascular risk factors are known to be influenced by feeding habits and life style changes which often vary between rural and urban settings. This study was aimed to investigate the relationship between cardiovascular risk factors and endothelial function in rural and urban children. Methods: A cross-sectional study on 6-9 years old children in randomly selected rural and urban schools of the Eastern Cape Province of South Arica was conducted. General anthropometric indices were measured followed by blood pressure (BP) measurements. The pulse wave velocity (PWV) was measured using a Vicorder. Urine sample was collected for the determination of albumin, creatinine, asymmetric dimethylarginine (ADMA), 8-hydroxy-2deoxyguanosine (8-OHdG) and thiobarbituric acid reactive substance (TBARS). Albumin to creatinine ratio (ACR) was calculated.Results: Children from urban settings (10.8%) had a higher prevalence of overweight/obesity than their rural counterparts (8.5%) while the prevalence of elevated/high blood pressure was higher in rural children (23.2%) than in urban children (19.0%). Diastolic blood pressure (DBP) and mean arterial blood pressure (MAP) significantly (p<0.005) increased with increasing quartiles of PWV. ADMA positively associated with HR in rural girls and showed a weak risk for elevated SBP and MAP. Body mass index (BMI) increased with increasing PWV and predicted endothelial dysfunction. 8-OHdG significantly (p<0.005) increased with increasing quartiles of ADMA and positively correlated with ADMA. Creatinine, albumin and ACR significantly (p<0.005) increased with increasing ADMA and ADMA associated positively with creatinine. Conclusion: Endothelial dysfunction was associated with obesity, high blood pressure, oxidative stress and microalbuminuria in children, and this relationship varied between rural and urban children.

show abstract

Endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication

Cited by 26 publications

References 90 publications

Augmented endothelial l‐arginine transport ameliorates pressure‐overload‐induced cardiac hypertrophy

Augmented endothelial l‐arginine transport ameliorates pressure‐overload‐induced cardiac hypertrophy

Novel Insights into the Role of HDL-Associated Sphingosine-1-Phosphate in Cardiometabolic Diseases

Cardiovascular Risk Factors and their Relationship with Endothelial Dysfunction in Rural and Urban South African Children

Contact Info

Product

Resources

About