Emerging role of TAK1 in the regulation of skeletal muscle mass

被引:2
|
作者
Roy, Anirban [1 ]
Narkar, Vihang A. [2 ]
Kumar, Ashok [1 ,3 ]
机构
[1] Univ Houston, Coll Pharm, Dept Pharmacol & Pharmaceut Sci, Houston, TX USA
[2] Univ Texas Hlth Sci Ctr, Brown Fdn Inst Mol Med, McGovern Med Sch, Houston, TX USA
[3] Univ Houston, Coll Pharm, Dept Pharmacol & Pharmaceut Sci, Hlth Bldg 2,Room 5012, Houston, TX 77204 USA
基金
美国国家卫生研究院;
关键词
hypertrophy; neuromuscular junctions; protein synthesis; signaling; skeletal muscle atrophy; TAK1; ACTIVATED KINASE 1; NF-KAPPA-B; TGF-BETA; PROTEIN-SYNTHESIS; MAMMALIAN TARGET; INDEPENDENT ACTIVATION; SIGNALING PATHWAYS; OXIDATIVE STRESS; MESSENGER-RNA; UP-REGULATION;
D O I
10.1002/bies.202300003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Maintenance of skeletal muscle mass and strength throughout life is crucial for heathy living and longevity. Several signaling pathways have been implicated in the regulation of skeletal muscle mass in adults. TGF-beta-activated kinase 1 (TAK1) is a key protein, which coordinates the activation of multiple signaling pathways. Recently, it was discovered that TAK1 is essential for the maintenance of skeletal muscle mass and myofiber hypertrophy following mechanical overload. Forced activation of TAK1 in skeletal muscle causes hypertrophy and attenuates denervation-induced muscle atrophy. TAK1-mediated signaling in skeletal muscle promotes protein synthesis, redox homeostasis, mitochondrial health, and integrity of neuromuscular junctions. In this article, we have reviewed the role and potential mechanisms through which TAK1 regulates skeletal muscle mass and growth. We have also proposed future areas of research that could be instrumental in exploring TAK1 as therapeutic target for improving muscle mass in various catabolic conditions and diseases.
引用
收藏
页数:12
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