Defects in lamin A-Prohibitin crosstalk leads to ROS elevation and OxPhos imbalance in laminocardiomyopathy
Subhradip Nath, Soumen K. Manna, Debasish Prusty, Sk Ramiz Islam, Kaushik Sengupta
This study shows that the lamin A K97E mutation disrupts PHB2 interaction, causing mitochondrial dysfunction, ROS elevation, and metabolic imbalance, contributing to dilated cardiomyopathy.
bioRxiv · Jul 17, 2025 · PreprintCell Biology