心力衰竭导致肌少症的分子机制

Cody A. Rutledge
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引用次数: 0

摘要

骨骼肌减少症又称 "肌肉疏松症",是一种与衰老相关的肌肉疾病,在心力衰竭(HF)患者中尤为常见。与整个心衰患者群体相比,患有肌肉疏松症的心衰患者预后较差。随着全球人口的老龄化,预计肌少症在心房颤动患者中的发病率只会越来越高,因此需要新的治疗策略来改善这一人群的预后。多种机理途径的出现可能解释了肌少症在心房颤动人群中发病率增加的原因,更好地了解这些途径可能有助于开发预防肌肉流失的疗法。这篇综述文章旨在探讨肌肉疏松症与高血压之间的分子机制,并讨论针对这些分子信号的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular mechanisms underlying sarcopenia in heart failure
The loss of skeletal muscle, also known as sarcopenia, is an aging-associated muscle disorder that is disproportionately present in heart failure (HF) patients. HF patients with sarcopenia have poor outcomes compared to the overall HF patient population. The prevalence of sarcopenia in HF is only expected to grow as the global population ages, and novel treatment strategies are needed to improve outcomes in this cohort. Multiple mechanistic pathways have emerged that may explain the increased prevalence of sarcopenia in the HF population, and a better understanding of these pathways may lead to the development of therapies to prevent muscle loss. This review article aims to explore the molecular mechanisms linking sarcopenia and HF, and to discuss treatment strategies aimed at addressing such molecular signals.
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