Increased Myostatin Activity and Decreased Myocyte Proliferation in Chronic Alcoholic Cardiomyopathy

Abstract

Alcohol produces cardiac myocyte loss through apoptosis but also partially inhibits myocyte proliferation through myostatin up-regulation. The final result may suppose an imbalance in myocyte homeostasis, with a net loss in total ventricular myocyte mass and progressive ventricular dysfunction.

Myostatin and insulin-like growth factor-1 in hypertensive heart disease

“…In a recent study by our group, we observed a non-significant downward trend of IGF-1 myocardial expression in AHT in human cardiac organ donors. Similarly, we have previously described the regulatory role of myostatin and IGF-1 in alcoholic CMP [13]. For the purpose of this study, myocardial samples were prospectively obtained from human heart donors and the effect of AHT on myostatin and IGF-1 myocardial expression was evaluated by immunohistochemistry.…”

“…Some of these patients had been included in previous studies on heart antioxidant status [31], cardiac apoptosis [32] and myostatin myocardial expression [13].…”

“…Its disruption causes increased skeletal and cardiac mass with myocyte hypertrophy and hyperplasia and increased proliferation [11,12]. In a previous study, we reported an increase in myostatin myocardium expression in patients with cardiomyopathy (CMP), either of alcoholic or other origin [13]. However, the specific role of myostatin in HHD has not been evaluated.…”

Alcoholic Cardiomyopathy: Old and New Insights

“…This is mediated by interference with myokines (FGF-21) and local hormones and growth-factors such as myostatin [33], IGF-1 [34], ghrelin [35] and leptin [36]. Thus, ethanol decreases the myocyte proliferation rate probably by myostatin up-regulation [33] and modifies the mechanisms of cardiac plasticity [37].…”

“…This is mediated by interference with myokines (FGF-21) and local hormones and growth-factors such as myostatin [33], IGF-1 [34], ghrelin [35] and leptin [36]. Thus, ethanol decreases the myocyte proliferation rate probably by myostatin up-regulation [33] and modifies the mechanisms of cardiac plasticity [37]. The final balance of alcoholinduced heart effects is a clear increase in the damaging factors and a decrease in protective heart mechanisms leading to progressive cardiac myocyte damage and loss by apoptosis and necrosis and the substitution of these cells by non-functional fibrosis [38,39].…”