Increased plasma myostatin in heart failure

Abstract

Aims Myostatin (Mstn), a member of the transforming growth factors (TGF)‐β family that regulate skeletal muscle growth, has been identified as a regulator of cardiomyocyte growth. The aim of our study was to measure Mstn plasma concentrations in patients with congestive heart failure (CHF) and to evaluate their relationship with other neurohormones released in CHF. Methods and results concentrations of Mstn were measured using a competitive immunoassay, in 76 CHF patients who were receiving optimal treatment and 60 healthy controls. Circulating levels of other neurohormones N‐terminal pro‐atrial natriuretic peptide (NT‐proANP), B‐type natriuretic peptide (BNP), N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP), and Big ET‐1 were also measured. Plasma Mstn was higher in CHF patients than in controls (63.0 vs. 43.0 ng/mL; P < 0.001). In CHF, Mstn levels correlated positively with NT‐proANP (r = 0.25; P = 0.03), BNP (r = 0.33; P < 0.01), NT‐proBNP (r = 0.32; P < 0.01), and Big ET‐1 (r = 0.26; P = 0.02). No significant correlations were observed with age and creatinine. Conclusion Our results demonstrate that plasma concentrations of Mstn are significantly increased in CHF patients and that Mstn correlates with biomarkers related to HF severity. Our study confirms the activation of Mstn in patients with heart failure.

Serum myostatin levels are independently associated with skeletal muscle wasting in patients with heart failure

“…[7] It was reported that plasma myostatin levels were shown to be increased in HF patients compared to in healthy controls. [8] However, this study has not reported the association between myostatin level and muscle wasting. On the other hand, in cardiac cachexia, characterized by a severe loss of skeletal muscle, weakness, and exercise intolerance, serum myostatin levels were decreased.…”

Sustained Elevation of Circulating Growth and Differentiation Factor-15 and a Dynamic Imbalance in Mediators of Muscle Homeostasis Are Associated With the Development of Acute Muscle Wasting Following Cardiac Surgery*

“…Despite a variety of muscle wasting conditions being associated with elevated levels of both muscle and plasma myostatin [8,10,11,[34][35][36], evidence from the acute phase of critical illness has been contradictory. For example, an increase in myostatin mRNA and protein from skeletal muscle of patients in the acute phase of critical illness has been reported [9], although this observation was not repeated in a more diverse population [32].…”

“…Myostatin, a member of the TGF-β superfamily, is a well recognised negative regulator of muscle mass [8], which has been implicated in the development of ICUAP. Elevation of both myostatin mRNA and protein was observed in the muscle of critically ill patients [9] and increased circulating levels of myostatin were observed in patients with muscle wasting associated with chronic obstructive pulmonary disease (COPD) [10], cardiac [11] and liver failure [12]. Other members of the TGF-β family also regulate muscle phenotype.…”

Serum myostatin levels are negatively associated with abdominal aortic calcification in older men: the STRAMBO study

“…For instance, inactivation of myostatin protects against the development of atherosclerosis in LDL receptor-deficient mice (5), and mechanical stress increases myocardial myostatin expression (6). In patients with heart failure, serum myostatin concentrations were increased compared with healthy controls in some, but not all, studies (7,8,9).…”