USP-48 enables insulin-mediated longevity and modulates the mitochondrial stress response.

Sergio Gordillo-García, Jesus Fernandez-Abascal, Blanca Hernando-Rodríguez, María Jesús Rodríguez-Palero, Laura Cantalejo-Carrasco, Aitor Jarit-Cabanillas, Manuel D Martínez-Bueno, Mercedes M Pérez-Jiménez, Enrique J Clavijo-Bernal, Aitana Cambón, Ildefonso Cases, Matthias Eder, Marta Artal-Sanz

Andalusian Centre for Developmental Biology, Consejo Superior de Investigaciones Científicas/Junta de Andalucía/Universidad Pablo de Olavide, Seville, Spain; Department of Molecular Biology and Biochemical Engineering, Universidad Pablo de Olavide, Seville, Spain.Andalusian Centre for Developmental Biology, Consejo Superior de Investigaciones Científicas/Junta de Andalucía/Universidad Pablo de Olavide, Seville, Spain; Department of Molecular Biology and Biochemical Engineering, Universidad Pablo de Olavide, Seville, Spain. · pubmed

Paper

Abstract

The mitochondrial prohibitin (PHB) complex is essential for mitochondrial homeostasis, yet its depletion produces opposite effects on lifespan: shortening it in wild-type C. elegans but extending it in insulin/IGF-1 receptor daf-2 mutants, which show an attenuated mitochondrial unfolded protein response (UPR

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

USP-48 enables insulin-mediated longevity by modulating the mitochondrial stress response, specifically the UPRmt, in C. elegans. This paper is relevant because it identifies a specific molecular mechanism (USP-48) that links the insulin/IGF-1 signaling pathway to mitochondrial homeostasis and lifespan regulation, providing a potential target for understanding how nutrient sensing controls aging.

Author of this paper? Send a correction.