mTOR inhibition triggers mitochondrial fragmentation in cardiomyocytes through proteosome-dependent prohibitin degradation and OPA-1 cleavage

mTOR inhibition triggers mitochondrial fragmentation in cardiomyocytes through proteosome-dependent prohibitin degradation and OPA-1 cleavage

Abstract Introduction Cardiac mitochondrial function is intricately regulated by various processes, ultimately impacting metabolic performance. Additionally, protein turnover is crucial for sustained metabolic homeostasis in cardiomyocytes. Objective Here, we studied the role of mTOR in OPA-1 cleava...

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Bibliographic Details
Main Authors: Hugo E. Verdejo, Valentina Parra, Andrea del Campo, Cesar Vasquez-Trincado, Damian Gatica, Camila Lopez-Crisosto, Jovan Kuzmicic, Leslye Venegas-Zamora, Ursula Zuñiga-Cuevas, Mayarling F. Troncoso, Rodrigo Troncoso, Beverly A. Rothermel, Mario Chiong, E. Dale Abel, Sergio Lavandero
Format: Article
Language:English
Published: BMC 2025-05-01
Series:Cell Communication and Signaling
Subjects:
mTOR
Rapamycin
Mitochondrial fusion
OPA-1
OMA1
Prohibitin
Online Access:https://doi.org/10.1186/s12964-025-02240-w
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