Univ. Lille, Univ. Artois, Univ. Littoral Côte d'Opale, ULR 7369 - URePSSS - Unité de Recherche Pluridisciplinaire Sport Santé Société, F-59000 Lille, France.
Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167 - RID-AGE - Facteurs de risque et déterminants moléculaires des maladies liées au vieillissement, F-59000 Lille, France.
Exp Gerontol. 2021 Apr;146:111247. doi: 10.1016/j.exger.2021.111247. Epub 2021 Jan 20.
Sarcopenia is characterized by a loss of muscle mass and function that reduces mobility, diminishes quality of life, and can lead to fall-related injuries. At the intracellular level, mitochondrial population alterations are considered as key contributors to the complex etiology of sarcopenia. Mitochondrial dysfunctions lead to reactive oxygen species production, altered cellular proteostasis, and promotes inflammation. Interestingly, the receptor for advanced glycation end-products (RAGE) is a pro-inflammatory receptor involved in inflammaging. In this review, after a brief description of sarcopenia, we will describe how mitochondria and the pathways controlling mitochondrial population quality could participate to age-induced muscle mass and force loss. Finally, we will discuss the RAGE-ligand axis during aging and its possible connection with mitochondria to control inflammaging and sarcopenia.
肌肉减少症的特征是肌肉质量和功能的丧失，这会降低活动能力，降低生活质量，并可能导致与跌倒相关的伤害。在细胞内水平上，线粒体群体的改变被认为是肌肉减少症复杂病因的关键因素。线粒体功能障碍导致活性氧的产生、细胞蛋白质稳态的改变，并促进炎症。有趣的是，晚期糖基化终产物受体 (RAGE) 是一种参与炎症老化的促炎受体。在简要描述肌肉减少症之后，我们将描述线粒体和控制线粒体群体质量的途径如何参与年龄引起的肌肉质量和力量丧失。最后，我们将讨论衰老过程中的 RAGE-配体轴及其与线粒体的可能联系，以控制炎症和肌肉减少症。
