DIAPH1-MFN2 interaction decreases the endoplasmic reticulum-mitochondrial distance and promotes cardiac injury following myocardial ischemia
Lorrie A. Kirshenbaum, Rimpy Dhingra, Roberto Bravo, Sergio Lavandero
Abstract
Contact between organelles such as the mitochondria (Mito) and endoplasmic reticulum (ER) is crucial to coordinate vital cellular homeostatic processes. Here we discuss recent work showing that Mito-ER proximity is regulated by heterotypic complexes between the F-actin polymerizing protein Diaphanous-1) and the mitochondrial dynamics protein Mitofusin 2, which confers increased susceptibility to ischemia/reperfusion injury.
Topics & Concepts
Endoplasmic reticulumCell biologyMFN2MitochondrionOrganelleIschemiaHomeostasisActinChemistryBiologyMedicinemitochondrial fusionBiochemistryInternal medicineMitochondrial DNAGeneMitochondrial Function and PathologyEndoplasmic Reticulum Stress and DiseaseATP Synthase and ATPases Research