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NLRP1 inflammasome modulates senescence and senescence-associated secretory phenotype

Muela-Zarzuela, I.; Suarez-Rivero, J. M.; Gallardo-Orihuela, A.; Wang, C.; Izawa, K.; de Gregorio-Procopio, M.; Couillin, I.; Ryffel, B.; Kitaura, J.; Sanz, A.; von Zglinicki, T.; Mbalaviele, G.; Cordero, M. D.

2023-02-10 immunology
10.1101/2023.02.06.527254 bioRxiv
Show abstract

Senescence is a cellular aging-related process triggered by different stresses and characterized by the secretion of various inflammatory factors referred to as the senescence-associated secretory phenotype (SASP). Here, we present evidence that the inflammasome sensor, NLRP1, is a key mediator of senescence induced by irradiation both in vitro and in vivo. The NLRP1 inflammasome promotes senescence by regulating the expression of p16, p21, p53, and SASP in Gasdermin D (GSDMD)-dependent manner as these responses are reduced in conditions of NLRP1 insufficiency or GSDMD inhibition. Mechanistically, the NLRP1 inflammasome is activated downstream of the cytosolic DNA sensor cGMP-AMP (cGAMP) synthase (cGAS) in response to genomic damage. These findings provide a rationale for inhibiting the NLRP1 inflammasome-GSDMD axis to treat senescence-driven disorders.

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"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.