Journal
CELL METABOLISM
Volume 32, Issue 1, Pages 87-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2020.05.002
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Funding
- Universite de Nice Sophia Antipolis
- Region Provence Alpes-Cote d'azur
- Conseil Departemental 06
- Gis Ibisa
- Canceropole PACA
- Region PACA
- l'INSERM
- ARC
- IBiSA
- Conseil Departemental 06 de la Region PACA
- Foundation ARC
- Agence Nationale de la Recherche (grant Senage'')
- Fondation Recherche Medicale
- Inserm Plan Cancer
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The accumulation of senescent cells can drive many age-associated phenotypes and pathologies. Consequently, it has been proposed that removing senescent cells might extend lifespan. Here, we generated two knockin mouse models targeting the best-characterizedmarker of senescence, p16(Ink4a). Using a genetic lineage tracing approach, we found that age-induced p16(High) senescence is a slow process that manifests around 10-12 months of age. The majority of p16(High) cells were vascular endothelial cells mostly in liver sinusoids (LSECs), and to lesser extent macrophages and adipocytes. In turn, continuous or acute elimination of p16(High) senescent cells disrupted blood-tissue barriers with subsequent liver and perivascular tissue fibrosis and health deterioration. Our data show that senescent LSECs are not replaced after removal and have important structural and functional roles in the aging organism. In turn, delaying senescence or replacement of senescent LSECs could represent a powerful tool in slowing down aging.
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