Rapamycin reveals neuropeptide Y as a regulator of senescence and inflammatory pathways in arthritis.

Susana Aideé González-Chávez, Eduardo Chaparro-Barrera, Mario Loya-Rivera, Alejandra Jazmín Rodríguez-Castillo, Rodrigo Prieto-Carrasco, Renato J Aguilera, Ana P Betancourt, Jonathon E Mohl, Daniel Alberto Ruizesparza-Hinojos, Sergio de Jesús Ramírez-Pérez, Mercedes Bermúdez, César Pacheco-Tena

PABIOM Laboratory, Faculty of Medicine and Biomedical Sciences, Autonomous University of Chihuahua, Chihuahua, Mexico. Electronic address: [email protected] Laboratory, Faculty of Medicine and Biomedical Sciences, Autonomous University of Chihuahua, Chihuahua, Mexico. Electronic address: [email protected]. · pubmed

Paper

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by immune dysregulation and joint destruction. Cellular senescence has been implicated in the progression of RA through the senescence-associated secretory phenotype (SASP), yet its molecular links to inflammation remain unclear. Rapamycin, an mTOR inhibitor with anti-inflammatory and anti-senescence properties, provides a valuable tool for exploring these mechanisms.

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Research summary

Rapamycin modulates neuropeptide Y to regulate senescence and inflammatory pathways in arthritis. The study addresses the role of cellular senescence in a chronic inflammatory disease, linking it to aging mechanisms and potential therapeutic interventions that could impact longevity.

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