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肌肉减少症:新出现的途径和潜在的药物靶点。

Muscle wasting: emerging pathways and potential drug targets.

机构信息

Department of Molecular Biology and Genetics, Koc University, Istanbul 34450, Turkey.

Department of Molecular Biology and Genetics, Koc University, Istanbul 34450, Turkey.

出版信息

Trends Pharmacol Sci. 2023 Oct;44(10):705-718. doi: 10.1016/j.tips.2023.07.006. Epub 2023 Aug 17.

DOI:10.1016/j.tips.2023.07.006
PMID:37596181
Abstract

Muscle wasting is a serious comorbidity associated with many disorders, including cancer, kidney disease, heart failure, and aging. Progressive loss of skeletal muscle mass negatively influences prognosis and survival, and is often accompanied by frailty and poor quality of life. Clinical trials testing therapeutics against muscle wasting have yielded limited success. Some therapies improved muscle mass in patients without appreciable differences in physical performance. This review article discusses emerging pathways that regulate muscle atrophy, including oncostatin M (OSM) and ectodysplasin A2 (EDA2) receptor (EDA2R) signaling, outcomes of recent clinical trials, and potential drug targets for future therapies.

摘要

肌肉减少症是一种与多种疾病相关的严重并发症,包括癌症、肾病、心力衰竭和衰老。骨骼肌进行性减少会对预后和生存产生负面影响,常伴有虚弱和生活质量下降。针对肌肉减少症的临床试验收效甚微。一些疗法改善了患者的肌肉质量,但对身体机能没有明显的改善。本文综述了调节肌肉萎缩的新途径,包括肿瘤坏死因子超家族成员 11(oncostatin M,OSM)和外胚层发育不良蛋白 A2 受体(ectodysplasin A2 receptor,EDA2R)信号通路、近期临床试验结果以及未来治疗的潜在药物靶点。

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