Molecular Pathogenesis of Sarcopenia: Regulatory Networks Involving MicroRNAs in Age-Related Skeletal Muscle Decline.

IF 3.1 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Joseph Joju Kalan, Lijo N Varghese, Rajesh Katare
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引用次数: 0

Abstract

Sarcopenia is the progressive loss of skeletal muscle mass, strength, and function, significantly contributing to frailty, disability, and mortality in aging populations. As life expectancy rises, sarcopenia presents a growing public health challenge, increasing healthcare costs, and diminishing quality of life. Despite its prevalence, sarcopenia is often underdiagnosed due to limitations in current diagnostic tools, including the lack of standardized cut-off values and reliance on physical performance tests. The causes of sarcopenia are multifactorial, involving oxidative stress, chronic inflammation, mitochondrial dysfunction, satellite cell depletion, and impaired angiogenesis. Recent research highlights the role of microRNAs (miRs) in regulating these molecular pathways. miRs influence muscle homeostasis by modulating gene expression related to muscle atrophy, apoptosis, inflammation, and insulin resistance. While non-pharmacological interventions such as resistance training and blood flow restriction therapy remain the primary treatment strategies, their effectiveness is often limited in older adults with reduced muscle regenerative capacity. The identification of miRs as biomarkers could enhance early diagnosis and enable more personalized treatment approaches. However, further research is required to validate their clinical utility and therapeutic potential. This review comprehensively analyses the molecular mechanisms underlying sarcopenia, current diagnostic challenges, and emerging miR-based strategies that could transform its management. Future efforts should focus on integrating these molecular insights into clinical practice to improve early detection and intervention strategies.

骨骼肌减少症的分子发病机制:涉及年龄相关骨骼肌衰退的microrna调控网络。
骨骼肌减少症是骨骼肌质量、力量和功能的逐渐丧失,是导致老年人虚弱、残疾和死亡的重要原因。随着预期寿命的增加,肌肉减少症带来了越来越大的公共卫生挑战,增加了医疗保健成本,降低了生活质量。尽管它很普遍,但由于目前诊断工具的局限性,包括缺乏标准化的临界值和依赖体能测试,肌肉减少症经常被误诊。肌肉减少症的病因是多因素的,包括氧化应激、慢性炎症、线粒体功能障碍、卫星细胞耗竭和血管生成受损。最近的研究强调了microrna (miRs)在调节这些分子通路中的作用。miRs通过调节与肌肉萎缩、细胞凋亡、炎症和胰岛素抵抗相关的基因表达来影响肌肉稳态。虽然抗阻训练和血流限制疗法等非药物干预措施仍然是主要的治疗策略,但它们在肌肉再生能力降低的老年人中往往效果有限。识别miRs作为生物标志物可以增强早期诊断,并使更个性化的治疗方法成为可能。然而,需要进一步的研究来验证它们的临床应用和治疗潜力。这篇综述全面分析了肌少症的分子机制,当前的诊断挑战,以及可能改变其管理的基于mir的新策略。未来的努力应该集中在将这些分子见解整合到临床实践中,以改善早期发现和干预策略。
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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