DIAPH1-MFN2 interaction decreases the endoplasmic reticulum-mitochondrial distance and promotes cardiac injury following myocardial ischemia

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 Diaphanou...

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Bibliographic Details
Published in:Nature communications 2024-02, Vol.15 (1), p.1469-1469, Article 1469
Main Authors: Kirshenbaum, Lorrie A., Dhingra, Rimpy, Bravo-Sagua, Roberto, Lavandero, Sergio
Format: Article
Language:English
Subjects:
631/80/86/1999
631/80/86/2366
Actin
Comment
Communication
Diabetes
Endoplasmic reticulum
Heart
Humanities and Social Sciences
Ischemia
Metabolism
Metabolites
Mitochondria
Morphology
multidisciplinary
Myocardial ischemia
Organelles
Polymerization
Proteins
Reperfusion
Science
Science (multidisciplinary)
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Summary: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.
ISSN:2041-1723
2041-1723
DOI:10.1038/s41467-024-45560-0