Myostatin: Twenty Years Later


如何引用文章

全文:

开放存取 开放存取
受限制的访问 ##reader.subscriptionAccessGranted##
受限制的访问 订阅存取

详细

In recent years, there has been an increasing interest in myostatin, a hormone that inhibits the growth and differentiation of muscle tissue. This interest is associated with an increase in the amount of data on the spectrum of the myostatin functioning. Myostatin, which has been known since 1997, belongs to the family of transforming growth factor β (TGF-β) and is a paracrine factor of skeletal muscle myocytes. It turned out that myostatin also affects the satellite cells and muscle fibroblasts, and its functions are not only to limit growth, but also to remodel skeletal muscles, which is necessary for muscle adaptation to physical training. Recent studies show that myostatin can play a significant role in musculoskeletal and cardiac cachexias in various pathologies, including cancer. It has been found that myostatin can be produced not only by skeletal muscle cells, but also by adipocytes and cardiomyocytes. It has been shown that, in cardiac pathology, the level of myostatin production increases in cardiac tissue. It is suggested that an increase in the myostatin production in the heart is necessary to prevent myocardial hypertrophy, which develops in some cardiac diseases. In this review, we examined the myostatin functions, as well as aspects of myostatin gene expression, mechanisms of its biosynthesis, its effect on various intracellular targets and transcription factors, and the regulation of its production. The importance of myostatin functions, as well as its involvement in pathological processes, allows us to consider this hormone as a promising target in therapeutic studies.

作者简介

D. Kostyunina

Moscow State University

编辑信件的主要联系方式.
Email: kostyunina.d@yandex.ru
俄罗斯联邦, Moscow

A. Ivanova

Moscow State University

Email: kostyunina.d@yandex.ru
俄罗斯联邦, Moscow

O. Smirnova

Moscow State University

Email: kostyunina.d@yandex.ru
俄罗斯联邦, Moscow


版权所有 © Pleiades Publishing, Inc., 2018
##common.cookie##