A review of mitochondrial dysfunction in diabetic sarcopenia: Mechanisms, diagnosis, and treatment approaches.

IF 1.5 4区 医学 Q4 MEDICINE, RESEARCH & EXPERIMENTAL
Journal of International Medical Research Pub Date : 2025-07-01 Epub Date: 2025-07-09 DOI:10.1177/03000605251355996
Zhilin Xie, Yuanhao Li, Xiaoliu Li, Jing Zhang
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引用次数: 0

Abstract

Diabetic sarcopenia is a common complication of diabetes, substantially impacting patients' quality of life and prognosis. Its pathogenesis is closely related to energy metabolism, with mitochondria-often referred to as the cellular "powerhouse"-playing a central role in this process. This review focuses on the role of mitochondrial dysfunction in diabetic sarcopenia, emphasizing mechanisms such as energy metabolism imbalance, oxidative stress-induced damage, and abnormalities in mitochondrial biogenesis and dynamics. Additionally, we discussed current research on diagnostic and therapeutic strategies targeting mitochondrial dysfunction. This narrative review aims to provide a theoretical foundation for a deeper understanding of the pathophysiology of diabetic sarcopenia and the development of novel therapeutic approaches.

糖尿病性肌肉减少症的线粒体功能障碍:机制、诊断和治疗方法综述。
糖尿病性肌肉减少症是糖尿病常见的并发症,严重影响患者的生活质量和预后。其发病机制与能量代谢密切相关,而线粒体——通常被称为细胞的“发电站”——在这一过程中起着核心作用。本文就线粒体功能障碍在糖尿病性肌肉减少症中的作用作一综述,强调其能量代谢失衡、氧化应激诱导的损伤以及线粒体生物发生和动力学异常等机制。此外,我们讨论了目前针对线粒体功能障碍的诊断和治疗策略的研究。本文旨在为深入了解糖尿病性肌肉减少症的病理生理学和开发新的治疗方法提供理论基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.20
自引率
0.00%
发文量
555
审稿时长
1 months
期刊介绍: _Journal of International Medical Research_ is a leading international journal for rapid publication of original medical, pre-clinical and clinical research, reviews, preliminary and pilot studies on a page charge basis. As a service to authors, every article accepted by peer review will be given a full technical edit to make papers as accessible and readable to the international medical community as rapidly as possible. Once the technical edit queries have been answered to the satisfaction of the journal, the paper will be published and made available freely to everyone under a creative commons licence. Symposium proceedings, summaries of presentations or collections of medical, pre-clinical or clinical data on a specific topic are welcome for publication as supplements. Print ISSN: 0300-0605
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