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T细胞中Bcl-xL的过表达可维持老年小鼠肌肉线粒体的结构和功能，并预防身体虚弱。

Bcl-xL overexpression in T cells preserves muscle mitochondrial structure and function and prevents frailty in old mice.

作者信息

Mas-Bargues Cristina, Román-Domínguez Aurora, Sanz-Ros Jorge, Romero-García Nekane, Huete-Acevedo Javier, Dromant Mar, Cuervo Ana María, Borrás Consuelo, Viña José

机构信息

Freshage Research Group, Department of Physiology, Faculty of Medicine, University of Valencia, Centro de Investigación Biomédica en Red Fragilidad y Envejecimiento Saludable-Instituto de Salud Carlos III (CIBERFES-ISCIII), INCLIVA, 46010 Valencia, Spain.

Department of Developmental and Molecular Biology, Institute for Aging Research, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

出版信息

Sci Adv. 2025 Mar 21;11(12):eadr1378. doi: 10.1126/sciadv.adr1378. Epub 2025 Mar 19.

DOI:10.1126/sciadv.adr1378
PMID:40106552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11922028/
Abstract

Our previous transcriptomic analysis revealed an up-regulation of the antiapoptotic protein B cell lymphoma-extra large (Bcl-xL) in centenarians relative to octogenarians or younger cohorts. In this study, we used Bcl-xL-overexpressing mice to assess its impact on successful aging. Our findings indicate that Bcl-xL overexpression modifies T cell subsets and improves their metabolism, apoptosis resistance, macroautophagy, and cytokine production during aging. This more resilient immune system reduces inflammation and preserves mitochondrial integrity and function in muscle tissue, thereby retarding the onset of frailty. These results underscore the important contribution of Bcl-xL to healthy aging, a phenomenon that is conserved across mammalian species.

摘要

我们之前的转录组分析显示，与八旬老人或更年轻的人群相比，百岁老人体内抗凋亡蛋白B细胞淋巴瘤-超大（Bcl-xL）上调。在本研究中，我们使用过表达Bcl-xL的小鼠来评估其对成功衰老的影响。我们的研究结果表明，Bcl-xL过表达可改变T细胞亚群，并改善其在衰老过程中的代谢、抗凋亡能力、巨自噬和细胞因子产生。这种更具弹性的免疫系统可减轻炎症，并维持肌肉组织中线粒体的完整性和功能，从而延缓衰弱的发生。这些结果强调了Bcl-xL对健康衰老的重要贡献，这一现象在哺乳动物物种中是保守的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766c/11922028/3f6e021321b6/sciadv.adr1378-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766c/11922028/4d82ea893cb7/sciadv.adr1378-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766c/11922028/3f6e021321b6/sciadv.adr1378-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766c/11922028/4d82ea893cb7/sciadv.adr1378-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766c/11922028/3f6e021321b6/sciadv.adr1378-f8.jpg

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本文引用的文献

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Am J Clin Exp Immunol. 2023 Dec 15;12(6):109-126. eCollection 2023.
2
Regulatory T cells shield muscle mitochondria from interferon-γ-mediated damage to promote the beneficial effects of exercise.调节性 T 细胞保护肌肉线粒体免受干扰素 -γ 介导的损伤，从而促进运动的有益作用。
Sci Immunol. 2023 Nov 3;8(89):eadi5377. doi: 10.1126/sciimmunol.adi5377.
3
Mitochondria pleiotropism in stem cell senescence: Mechanisms and therapeutic approaches.
线粒体在干细胞衰老中的多效性：机制与治疗方法。
Free Radic Biol Med. 2023 Nov 1;208:657-671. doi: 10.1016/j.freeradbiomed.2023.09.019. Epub 2023 Sep 20.
4
Age-associated inflammation and implications for skeletal muscle responses to exercise.与年龄相关的炎症与运动对骨骼肌反应的影响。
Exp Gerontol. 2023 Jun 15;177:112177. doi: 10.1016/j.exger.2023.112177. Epub 2023 May 2.
5
Mitochondrial dynamics maintain muscle stem cell regenerative competence throughout adult life by regulating metabolism and mitophagy.线粒体动态平衡通过调节代谢和自噬来维持肌肉干细胞的再生能力，贯穿成年生活。
Cell Stem Cell. 2022 Sep 1;29(9):1298-1314.e10. doi: 10.1016/j.stem.2022.07.009. Epub 2022 Aug 22.
6
Regulatory T cells-centered regulatory networks of skeletal muscle inflammation and regeneration.以调节性T细胞为中心的骨骼肌炎症与再生调节网络。
Cell Biosci. 2022 Jul 22;12(1):112. doi: 10.1186/s13578-022-00847-x.
7
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Front Aging. 2022 May 2;3:870489. doi: 10.3389/fragi.2022.870489. eCollection 2022.
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Nat Rev Endocrinol. 2022 Apr;18(4):243-258. doi: 10.1038/s41574-021-00626-7. Epub 2022 Feb 10.
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Front Physiol. 2021 Aug 20;12:668327. doi: 10.3389/fphys.2021.668327. eCollection 2021.
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