TERT expression attenuates metabolic disorders in obese mice by promoting adipose stem and progenitor cell expansion and differentiation.

Laura Braud, Manuel Bernabe, Julien Vernerey, Antonio M A Miranda, Andrea Dominguez, Dmitri Churikov, Manon Richaud, Frédéric Jourquin, Liam Mc Allan, Christophe Lachaud, Jesus Gil, Will Scott, Vincent Géli

Marseille Cancer Research Centre (CRCM), U1068 INSERM, UMR7258 CNRS, UM105 Aix-Marseille University, Institut Paoli-Calmettes, Marseille, France. Ligue Nationale Contre le Cancer (Equipe Labellisée). Electronic address: [email protected]. · pubmed

Paper

Abstract

Adipose tissue (AT) senescence, induced by obesity or aging, leads to a reduced capacity for tissue remodeling and a chronic pro-inflammatory state, which leads to the onset of metabolic pathologies. Cellular senescence is triggered by various stresses, in particular excessive shortening of telomeres, which activates the p21 pathway and leads to the arrest of the cell cycle. We used the mouse model p21

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Research summary

TERT expression promotes the expansion and differentiation of adipose stem and progenitor cells, which may mitigate metabolic disorders associated with obesity. This research addresses cellular senescence and its role in metabolic dysfunction, linking it to the broader context of aging and longevity.

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