| First Author | Desdín-Micó G | Year | 2020 |
| Journal | Science | Volume | 368 |
| Issue | 6497 | Pages | 1371-1376 |
| PubMed ID | 32439659 | Mgi Jnum | J:290821 |
| Mgi Id | MGI:6436812 | Doi | 10.1126/science.aax0860 |
| Citation | Desdin-Mico G, et al. (2020) T cells with dysfunctional mitochondria induce multimorbidity and premature senescence. Science 368(6497):1371-1376 |
| abstractText | 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-alpha 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. |
