骨骼肌
蛋白质降解
内分泌学
肌肉萎缩
内科学
脱碘酶
肌发生
蛋白质周转
三碘甲状腺素
萎缩
生物
甲状腺
泛素
激素
化学
细胞生物学
生物化学
医学
蛋白质生物合成
基因
作者
Maria Angela De Stefano,Raffaele Ambrosio,Tommaso Porcelli,Gianfranco Orlandino,Domenico Salvatore,Cristina Luongo
出处
期刊:Metabolites
[MDPI AG]
日期:2021-10-25
卷期号:11 (11): 730-730
被引量:8
标识
DOI:10.3390/metabo11110730
摘要
Skeletal muscle atrophy is a condition associated with various physiological and pathophysiological conditions, such as denervation, cachexia, and fasting. It is characterized by an altered protein turnover in which the rate of protein degradation exceeds the rate of protein synthesis, leading to substantial muscle mass loss and weakness. Muscle protein breakdown reflects the activation of multiple proteolytic mechanisms, including lysosomal degradation, apoptosis, and ubiquitin–proteasome. Thyroid hormone (TH) plays a key role in these conditions. Indeed, skeletal muscle is among the principal TH target tissue, where TH regulates proliferation, metabolism, differentiation, homeostasis, and growth. In physiological conditions, TH stimulates both protein synthesis and degradation, and an alteration in TH levels is often responsible for a specific myopathy. Intracellular TH concentrations are modulated in skeletal muscle by a family of enzymes named deiodinases; in particular, in muscle, deiodinases type 2 (D2) and type 3 (D3) are both present. D2 activates the prohormone T4 into the active form triiodothyronine (T3), whereas D3 inactivates both T4 and T3 by the removal of an inner ring iodine. Here we will review the present knowledge of TH action in skeletal muscle atrophy, in particular, on the molecular mechanisms presiding over the control of intracellular T3 concentration in wasting muscle conditions. Finally, we will discuss the possibility of exploiting the modulation of deiodinases as a possible therapeutic approach to treat muscle atrophy.
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