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Título: | T cells with dysfunctional mitochondria induce multimorbidity and premature senescence |
Autor: | Desdín-Mico, Gabriela; Soto-Heredero, Gonzalo; Aranda, Juan Francisco CSIC ORCID; Oller, Jorge; Carrasco, Elisa CSIC ORCID; Gabandé-Rodríguez, Enrique; Blanco, Eva M.; Alfranca, Arantzazu; Cussó, Lorena; Desco, Manuel; Ibañez, Borja; Gortazar, Arancha R.; Fernández-Marcos, Pablo; Navarro, María N. CSIC ORCID; Hernaez, Bruno; Alcamí, Antonio CSIC ORCID; Baixauli, Francesc; Mittelbrunn, María CSIC ORCID CVN | Fecha de publicación: | 21-may-2020 | Editor: | American Association for the Advancement of Science | Citación: | Science 368(6497): 1371-1376 (2020) | Resumen: | The effect of immunometabolism on age-associated diseases remains uncertain. In this work, we show that T cells with dysfunctional mitochondria owing to mitochondrial transcription factor A (TFAM) deficiency act as accelerators of senescence. In mice, these cells instigate multiple aging-related features, including metabolic, cognitive, physical, and cardiovascular alterations, which together result in premature death. T cell metabolic failure induces the accumulation of circulating cytokines, which resembles the chronic inflammation that is characteristic of aging (“inflammaging”). This cytokine storm itself acts as a systemic inducer of senescence. Blocking tumor necrosis factor-a signaling or preventing senescence with nicotinamide adenine dinucleotide precursors partially rescues premature aging in mice with Tfam-deficient T cells. Thus, T cells can regulate organismal fitness and life span, which highlights the importance of tight immunometabolic control in both aging and the onset of age-associated diseases. | Versión del editor: | http://dx.doi.org/10.1126/science.aax0860 | URI: | http://hdl.handle.net/10261/342328 | DOI: | 10.1126/science.aax0860 | Identificadores: | doi: 10.1126/science.aax0860 e-issn: 1095-9203 issn: 0036-8075 |
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