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顺铂诱导的肌肉消耗与萎缩:分子机制及潜在治疗干预措施

Cisplatin-Induced Muscle Wasting and Atrophy: Molecular Mechanism and Potential Therapeutic Interventions.

作者信息

Huang Ko-Chieh, Chiang Yi-Fen, Ali Mohamed, Hsia Shih-Min

机构信息

School of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei, Taiwan.

Clinical Pharmacy Department, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.

出版信息

J Cachexia Sarcopenia Muscle. 2025 Jun;16(3):e13817. doi: 10.1002/jcsm.13817.

DOI:10.1002/jcsm.13817
PMID:40343378
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12059472/
Abstract

Platinum-based chemotherapeutics, particularly cisplatin, are crucial in the treatment of various malignancies due to their strong antitumor effects. However, a significant side effect of cisplatin is muscle atrophy, which severely impairs physical strength, diminishes quality of life and complicates cancer therapy. Cisplatin-induced muscle wasting arises from a complex interplay of enhanced proteolysis, reduced muscle protein synthesis and systemic inflammation. Understanding the underlying molecular mechanisms of muscle atrophy is vital for identifying new therapeutic targets. This review systematically explores molecular-based therapies and plant-derived natural compounds, providing a comprehensive overview of their efficacy in vivo and in vitro for preventing cisplatin-induced muscle atrophy. Both molecular-based therapies and plant-derived natural compounds present promising strategies for mitigating cisplatin-induced muscle atrophy. Ghrelin, growth hormone secretagogues and testosterone stimulate anabolic pathways and reduce muscle degradation, whereas natural compounds like capsaicin and naringenin exert protective effects by reducing inflammation and oxidative stress. A better understanding of the pathophysiology of muscle atrophy, combined with optimized therapeutic applications, may facilitate the clinical translation of these interventions to improve outcomes for cancer patients undergoing chemotherapy.

摘要

铂类化疗药物,尤其是顺铂,因其强大的抗肿瘤作用,在各种恶性肿瘤的治疗中至关重要。然而,顺铂的一个显著副作用是肌肉萎缩,这严重损害体力、降低生活质量并使癌症治疗复杂化。顺铂诱导的肌肉萎缩源于蛋白水解增强、肌肉蛋白合成减少和全身炎症的复杂相互作用。了解肌肉萎缩的潜在分子机制对于确定新的治疗靶点至关重要。本综述系统地探讨了基于分子的疗法和植物来源的天然化合物,全面概述了它们在体内和体外预防顺铂诱导的肌肉萎缩的疗效。基于分子的疗法和植物来源的天然化合物都为减轻顺铂诱导的肌肉萎缩提供了有前景的策略。胃饥饿素、生长激素促分泌素和睾酮刺激合成代谢途径并减少肌肉降解,而辣椒素和柚皮苷等天然化合物通过减轻炎症和氧化应激发挥保护作用。更好地理解肌肉萎缩的病理生理学,结合优化的治疗应用,可能有助于将这些干预措施转化为临床应用,以改善接受化疗的癌症患者的预后。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1abf/12059472/673818f3301d/JCSM-16-e13817-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1abf/12059472/d60f27bf6531/JCSM-16-e13817-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1abf/12059472/a368e6f55dd3/JCSM-16-e13817-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1abf/12059472/2dcbc64aeef9/JCSM-16-e13817-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1abf/12059472/673818f3301d/JCSM-16-e13817-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1abf/12059472/d60f27bf6531/JCSM-16-e13817-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1abf/12059472/a368e6f55dd3/JCSM-16-e13817-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1abf/12059472/2dcbc64aeef9/JCSM-16-e13817-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1abf/12059472/673818f3301d/JCSM-16-e13817-g001.jpg

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Taurine Prevents Angiotensin II-Induced Human Endocardial Endothelium Morphological Remodeling and the Increase in Cytosolic and Nuclear Calcium and ROS.牛磺酸可预防血管紧张素II诱导的人心脏内膜内皮细胞形态重塑以及细胞溶质和细胞核钙及活性氧的增加。
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