肌肉消耗是许多疾病的严重并发症，包括癌症、肾脏疾病、心力衰竭和衰老。骨骼肌质量的逐渐丧失对预后和生存率产生负面影响，并且常常伴随虚弱和生活质量差。对抗肌肉消耗的临床试验取得了有限的成功。一些治疗方法在患者中改善了肌肉质量，但在体力表现方面几乎没有明显差异。本综述文章讨论了调控肌肉萎缩的新途径，包括癌细胞生成素M（OSM）和外胚层发育异常蛋白A2（EDA2）受体（EDA2R）信号传导、近期临床试验的结果以及未来治疗的潜在药物靶点。版权所有 © 2023 Elsevier Ltd. 保留所有权利。

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.Copyright © 2023 Elsevier Ltd. All rights reserved.