Cisplatin-Induced Skeletal Muscle Atrophy: Biomolecular Mechanisms and the Protective Role of Exercise-Induced Myokines

TL;DR

Cisplatin chemotherapy causes muscle loss, but exercise may help by boosting protective muscle proteins called myokines.

Contribution

This review highlights how exercise-induced myokines protect against cisplatin-induced muscle atrophy.

Findings

Cisplatin causes muscle atrophy through oxidative stress and inflammation.

Exercise activates myokines like IL-6 and irisin to reduce muscle damage.

Exercise improves metabolic and immune health while promoting muscle repair.

Abstract

Cisplatin is a widely used chemotherapy drug for the treatment of various cancers; however, its clinical use is often accompanied by skeletal muscle atrophy, which not only impacts patients’ physical health but also significantly diminishes their quality of life. The mechanisms underlying cisplatin-induced muscle atrophy are complex and involve a series of molecular biological processes, including oxidative stress, inflammation, protein degradation, and muscle cell apoptosis. Recent studies have suggested that exercise intervention can significantly alleviate cisplatin-induced muscle damage by modulating exercise-induced myokines. Myokines, such as muscle-derived cytokines (e.g., IL-6, irisin) and other related factors, can mitigate muscle atrophy through anti-inflammatory, antioxidative, and muscle-synthesis-promoting mechanisms. This review explores the molecular mechanisms of cisplatin-induced skeletal muscle atrophy, examines the potential protective effects of exercise intervention, and highlights the role of exercise-induced myokines in this process. The findings suggest that exercise not only alleviates chemotherapy-induced muscle atrophy by improving metabolic and immune status but also activates myokines to promote muscle regeneration and repair, offering a promising adjunctive therapy for cisplatin-treated patients.

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