Abstract
The primary role of myostatin is to negatively regulate skeletal muscle growth. The gait speed is a noninvasive, reliable parameter that predicts cardiovascular risk and mortality. This study evaluated the relationship between serum myostatin concentrations and gait speeds in patients who had undergone kidney transplantation (KT). A total of 84 KT recipients were evaluated. A speed of less than 1.0 m/s was categorized into the low gait speed group. We measured serum myostatin concentrations with a commercial enzyme-linked immunosorbent assay. KT recipients in the low gait speed group had significantly older age, as well as higher body weight, body mass index (BMI), skeletal muscle index, serum triglyceride levels, glucose levels, and blood urea nitrogen levels, lower estimated glomerular filtration rates and serum myostatin levels, a higher percentage of steroid use, and a lower proportion of mycophenolate mofetil use. Multivariable logistic regression analysis revealed that lower myostatin levels and lower frequency of mycophenolate mofetil use were independently associated with low gait speed. In multivariable stepwise linear regression analysis, myostatin levels were positively correlated with gait speeds, and age and BMI were negatively correlated with gait speeds. In the study, serum myostatin levels were significantly lower in the low gait speed group. Subjects in the low gait speed group also had greater BMI and older age.
Highlights
Publisher’s Note: MDPI stays neutralMyostatin, a member of the transforming growth factor-β (TGF-β) superfamily, is a negative regulator of skeletal muscle development and growth [1]
We aimed to evaluate the association between gait speed and serum myostatin levels in kidney transplantation (KT) recipients
The most important finding is that lower serum myostatin levels, older age, and higher body mass index (BMI) were independently associated with low gait speeds in KT recipi
Summary
A member of the transforming growth factor-β (TGF-β) superfamily, is a negative regulator of skeletal muscle development and growth [1]. It is predominantly produced in skeletal muscles in response to various factors, including inflammatory cytokines, oxidative stress, ammonia, angiotensin II, and glucocorticoids [2]. Myostatin up-regulates p21 (a cyclin-dependent kinase inhibitor) and decreases cyclin-dependent kinase 2 (Cdk2) protein levels and activity in myoblasts, inhibiting myoblasts from G1 to S phase of the cell cycle [4]. Treatment of sarcopenia with bimagrumab, a human monoclonal antibody against type II activin receptors, causing them to act as myostatin inhibitors, increased skeletal muscle mass and strength and increased walking speeds [6]. It was found that with regard to jurisdictional claims in published maps and institutional affiliations
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