2026-09-15T07:27:21Zhttps://gredos.usal.es/oai/request

oai:gredos.usal.es:10366/1667502025-08-01T00:01:42Zcom_10366_3966com_10366_3947com_10366_3946com_10366_3823col_10366_3967

Covarrubias, Anthony J Kale, Abhijit Perrone, Rosalba López Domínguez, José Alberto Pisco, Angela Oliveira Kasler, Herbert G Schmidt, Mark S Heckenbach, Indra Kwok, Ryan Wiley, Christopher D Wong, Hoi-Shan Gibbs, Eddy Iyer, Shankar S Basisty, Nathan Wu, Qiuxia Kim, Ik-Jung Silva, Elena Vitangcol, Kaitlyn Shin, Kyong-Oh Lee, Yong-Moon Riley, Rebeccah Ben-Sahra, Issam Ott, Melanie Schilling, Birgit Scheibye-Knudsen, Morten Ishihara, Katsuhiko Quake, Stephen R Newman, John Brenner, Charles Campisi, Judith Verdin, Eric 2020-11 [EN]Declining tissue nicotinamide adenine dinucleotide (NAD) levels are linked to ageing and its associated diseases. However, the mechanism for this decline is unclear. Here, we show that pro-inflammatory M1-like macrophages, but not naive or M2 macrophages, accumulate in metabolic tissues, including visceral white adipose tissue and liver, during ageing and acute responses to inflammation. These M1-like macrophages express high levels of the NAD-consuming enzyme CD38 and have enhanced CD38-dependent NADase activity, thereby reducing tissue NAD levels. We also find that senescent cells progressively accumulate in visceral white adipose tissue and liver during ageing and that inflammatory cytokines secreted by senescent cells (the senescence-associated secretory phenotype, SASP) induce macrophages to proliferate and express CD38. These results uncover a new causal link among resident tissue macrophages, cellular senescence and tissue NAD decline during ageing and offer novel therapeutic opportunities to maintain NAD levels during ageing. http://hdl.handle.net/10366/166750 eng 2302 Bioquímica 2415 Biología Molecular Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages. info:eu-repo/semantics/article TEXT Gredos. Repositorio Documental de la Universidad de Salamanca Hispana