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骨骼肌铁稳态的年龄相关变化。

Age-Related Changes in Skeletal Muscle Iron Homeostasis.

作者信息

Alves Francesca M, Ayton Scott, Bush Ashley I, Lynch Gordon S, Koopman René

机构信息

Centre for Muscle Research, Department of Anatomy and Physiology, The University of Melbourne, Victoria, Australia.

Melbourne Dementia Research Centre, The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.

出版信息

J Gerontol A Biol Sci Med Sci. 2023 Jan 26;78(1):16-24. doi: 10.1093/gerona/glac139.

DOI:10.1093/gerona/glac139
PMID:35869751
Abstract

Sarcopenia is an age-related condition of slow, progressive loss of muscle mass and strength, which contributes to frailty, increased risk of hospitalization and mortality, and increased health care costs. The incidence of sarcopenia is predicted to increase to >200 million affected older adults worldwide over the next 40 years, highlighting the urgency for understanding biological mechanisms and developing effective interventions. An understanding of the mechanisms underlying sarcopenia remains incomplete. Iron in the muscle is important for various metabolic functions, including oxygen supply and electron transfer during energy production, yet these same chemical properties of iron may be deleterious to the muscle when either in excess or when biochemically unshackled (eg, in ferroptosis), it can promote oxidative stress and induce inflammation. This review outlines the mechanisms leading to iron overload in muscle with aging and evaluates the evidence for the iron overload hypothesis of sarcopenia. Based on current evidence, studies are needed to (a) determine the mechanisms leading to iron overload in skeletal muscle during aging; and (b) investigate whether skeletal muscles are functionally deficient in iron during aging leading to impairments in oxidative metabolism.

摘要

肌肉减少症是一种与年龄相关的病症,表现为肌肉质量和力量缓慢、渐进性丧失,这会导致身体虚弱、住院风险和死亡率增加,以及医疗保健成本上升。预计在未来40年内,全球肌肉减少症的发病率将增至超过2亿受影响的老年人,这凸显了理解其生物学机制并开发有效干预措施的紧迫性。对肌肉减少症潜在机制的理解仍不完整。肌肉中的铁对于各种代谢功能很重要,包括能量产生过程中的氧气供应和电子传递,然而,铁的这些相同化学性质在过量或生化不受束缚时(例如在铁死亡中)可能对肌肉有害,它会促进氧化应激并引发炎症。本综述概述了随着年龄增长导致肌肉中铁过载的机制,并评估了肌肉减少症铁过载假说的证据。基于目前的证据,需要开展研究以:(a)确定衰老过程中导致骨骼肌铁过载的机制;以及(b)研究衰老过程中骨骼肌是否在功能上缺铁,从而导致氧化代谢受损。

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