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

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  • Lorrie A. Kirshenbaum

    (The Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Department of Physiology and Pathophysiology
    University of Manitoba)

  • Rimpy Dhingra

    (The Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Department of Physiology and Pathophysiology
    University of Manitoba)

  • Roberto Bravo-Sagua

    (Universidad de Chile
    Consortium of Universities of the State of Chile (CUECH)
    University of Chile)

  • Sergio Lavandero

    (University of Chile
    University of Texas Southwestern Medical Center)

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.

Suggested Citation

  • Lorrie A. Kirshenbaum & Rimpy Dhingra & Roberto Bravo-Sagua & Sergio Lavandero, 2024. "DIAPH1-MFN2 interaction decreases the endoplasmic reticulum-mitochondrial distance and promotes cardiac injury following myocardial ischemia," Nature Communications, Nature, vol. 15(1), pages 1-3, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-45560-0
    DOI: 10.1038/s41467-024-45560-0
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    References listed on IDEAS

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    1. Gautham Yepuri & Lisa M. Ramirez & Gregory G. Theophall & Sergei V. Reverdatto & Nosirudeen Quadri & Syed Nurul Hasan & Lei Bu & Devi Thiagarajan & Robin Wilson & Raquel López Díez & Paul F. Gugger & , 2023. "DIAPH1-MFN2 interaction regulates mitochondria-SR/ER contact and modulates ischemic/hypoxic stress," Nature Communications, Nature, vol. 14(1), pages 1-25, December.
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