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

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

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.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. · pubmed

Paper

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.

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Research summary

Bcl-xL overexpression in T cells enhances immune function and mitochondrial integrity, thereby delaying frailty in aging mice. This study addresses mechanisms that contribute to healthy aging, focusing on the preservation of cellular function and resilience in the context of aging.

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