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肌肉减少症和恶病质:分子机制与治疗干预

Sarcopenia and cachexia: molecular mechanisms and therapeutic interventions.

作者信息

Wang Tiantian, Zhou Dong, Hong Zhen

机构信息

Department of Neurology West China Hospital of Sichuan University Chengdu Sichuan China.

Institute of Brain Science and Brain-Inspired Technology of West China Hospital Sichuan University Chengdu Sichuan China.

出版信息

MedComm (2020). 2025 Jan 5;6(1):e70030. doi: 10.1002/mco2.70030. eCollection 2025 Jan.

DOI:10.1002/mco2.70030
PMID:39764565
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11702502/
Abstract

Sarcopenia is defined as a muscle-wasting syndrome that occurs with accelerated aging, while cachexia is a severe wasting syndrome associated with conditions such as cancer and immunodeficiency disorders, which cannot be fully addressed through conventional nutritional supplementation. Sarcopenia can be considered a component of cachexia, with the bidirectional interplay between adipose tissue and skeletal muscle potentially serving as a molecular mechanism for both conditions. However, the underlying mechanisms differ. Recognizing the interplay and distinctions between these disorders is essential for advancing both basic and translational research in this area, enhancing diagnostic accuracy and ultimately achieving effective therapeutic solutions for affected patients. This review discusses the muscle microenvironment's changes contributing to these conditions, recent therapeutic approaches like lifestyle modifications, small molecules, and nutritional interventions, and emerging strategies such as gene editing, stem cell therapy, and gut microbiome modulation. We also address the challenges and opportunities of multimodal interventions, aiming to provide insights into the pathogenesis and molecular mechanisms of sarcopenia and cachexia, ultimately aiding in innovative strategy development and improved treatments.

摘要

肌肉减少症被定义为一种随着衰老加速而出现的肌肉萎缩综合征,而恶病质是一种与癌症和免疫缺陷疾病等病症相关的严重消瘦综合征,传统营养补充无法完全解决该问题。肌肉减少症可被视为恶病质的一个组成部分,脂肪组织与骨骼肌之间的双向相互作用可能是这两种病症的分子机制。然而,其潜在机制有所不同。认识到这些疾病之间的相互作用和区别对于推进该领域的基础研究和转化研究、提高诊断准确性并最终为受影响患者实现有效的治疗方案至关重要。本综述讨论了导致这些病症的肌肉微环境变化、近期的治疗方法,如生活方式改变、小分子和营养干预,以及新兴策略,如基因编辑、干细胞疗法和肠道微生物群调节。我们还探讨了多模式干预的挑战和机遇,旨在深入了解肌肉减少症和恶病质的发病机制和分子机制,最终有助于创新策略的开发和改进治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c1/11702502/f2f6e6e6b860/MCO2-6-e70030-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c1/11702502/e0546fe80aec/MCO2-6-e70030-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c1/11702502/55c9e905eaee/MCO2-6-e70030-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c1/11702502/ad968b6d3a03/MCO2-6-e70030-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c1/11702502/cac771391136/MCO2-6-e70030-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c1/11702502/f2f6e6e6b860/MCO2-6-e70030-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c1/11702502/e0546fe80aec/MCO2-6-e70030-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c1/11702502/55c9e905eaee/MCO2-6-e70030-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c1/11702502/ad968b6d3a03/MCO2-6-e70030-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c1/11702502/cac771391136/MCO2-6-e70030-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c1/11702502/f2f6e6e6b860/MCO2-6-e70030-g004.jpg

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本文引用的文献

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Adipose tissue in older individuals: a contributing factor to sarcopenia.老年人的脂肪组织:肌少症的一个促成因素。
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