T细胞中Bcl-xL的过表达可保持老年小鼠肌肉线粒体的结构和功能并预防其衰弱

 Overexpression of Bcl‑xL in T‑cells preserves mitochondrial structure and function in skeletal muscle and prevents frailty in aged mice.

关键词：T细胞、肌肉线粒体

Keywords: T cells, muscle mitochondria

作者：Cristina Mas-Bargues^1,2†, Aurora Román-Domínguez¹†,Jorge Sanz-Ros¹‡,Nekane Romero-García¹§,Javier Huete-Acevedo¹, Mar Dromant¹, Ana María Cuervo², Consuelo Borrás¹*, JoséViña¹

摘要：基于百岁老人T细胞中含有高表达Bcl-xL的前期发现，本研究构建T细胞特异性过表达Bcl-xL的转基因小鼠模型，通过一系列实验证实Bcl-xL可改善衰老T细胞的代谢效率、抗凋亡能力、自噬水平并降低促炎因子（IL-1β、TNF-α、IFN-γ）分泌；促进调节性T 细胞（Treg）向骨骼肌浸润、抑制IFN-γ介导的炎症，维持老年小鼠肌肉线粒体结构与功能，最终延缓肌少症、降低衰弱发生率。

Abstract: Based on our previous finding that T cells from centenarians exhibit high Bcl‑xL expression, this study generated a transgenic mouse model with T‑cell‑specific overexpression of Bcl‑xL. A series of experiments demonstrated that Bcl‑xL improves metabolic efficiency, anti‑apoptotic capacity and autophagy levels in aged T cells, and reduces the secretion of pro‑inflammatory cytokines (IL‑1β, TNF‑α, IFN‑γ). Moreover, Bcl‑xL promotes the infiltration of regulatory T cells (Tregs) into skeletal muscle, suppresses IFN‑γ‑mediated inflammation, preserves the structural and functional integrity of muscle mitochondria in aged mice, and ultimately delays sarcopenia and reduces the incidence of frailty.

点击链接即可查看文章：https://www.science.org/doi/10.1126/sciadv.adr1378

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