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Myostatin (GDF-8) is a major regulatory factor on cardiac metabolism, function and energy homeostasis. Although the main site for myostatin expression is the skeletal muscle, it has a relevant role in heart pathophysiology. Myostatin up-regulation inhibits cardiac myocyte proliferation and protects the cell from apoptosis. Myostatin disruption induces myocyte hyperplasia, hypertrophy and proliferation, increasing global cardiac mass. Myostatin up-regulation appears after different pathological heart conditions such as ventricular hypertrophy and chronic heart failure.  

Alcohol misuse up-regulates myostatin cardiac expression, a fact similar to that happens in hypertension or other causes of cardiomyopathy (CMP). In the case of chronic alcoholics, this myostatin up-regulation is higher and the heart proliferation ratio lower compared to other groups with CMP.  In the presence of isolated hypertension myocardial myostatin activity is not modified, but in hypertensive CMP, heart myostatin expression is clearly increased.

The presence of structural dilated CMP induces a significant increase in heart myostatin expression independently of their etiology, either in alcoholic, hypertensive, valve, ischemic or idiopathic CMP.  In the setting of heart failure, myostatin expression is also up-regulated independently of their etiologic cause, especially in end-stage heart failure. Myostatin up-regulation probably appears to limit the compensatory but excessive cardiac growth. It contributes to restrict unhealthy repair mechanisms mostly myocyte hypertrophy and proliferation and also regulates heart energy homeostasis.

In addition to myostatin, other novel cardiomyokines such as IGF-1, FGF21 and Metrnl appear to have a relevant role in regulation of cardiac hypertrophy and remodelling. These cardiomyokines have also been proposed as diagnostic markers and potential therapeutic agents.

In alcohol and hypertensive heart diseases, in addition to decrease heart aggressive factors (alcohol intake, hypertension overload), control of local cardiac neuro-hormonal pathways will be relevant points to consider in the future.