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Targeting of CIP4-Calcineurin Signalosomes Improves Cardiac Structure and Function After Myocardial Infarction.

Anne-Maj Samuelsson, Abraham L Bayer, Jinliang Li

    Biorxiv : the Preprint Server for Biology
    |June 4, 2025
    PubMed
    Summary

    Targeting Cdc42-interacting protein 4 (CIP4) signalosomes improves cardiac function in mice with myocardial infarction and ischemic cardiomyopathy. Gene therapy using a calcineurin Aβ-derived peptide shows promise for treating these cardiovascular conditions.

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    Area of Science:

    • Cardiovascular Research
    • Molecular Cardiology
    • Gene Therapy

    Background:

    • Calcineurin is a signaling enzyme with dual roles in cardiac remodeling and cardioprotection, complicating its therapeutic use.
    • Cdc42-interacting protein 4 (CIP4) organizes calcineurin Aβ2 (CaNAβ2) signaling compartments, independent of contractile calcium.
    • Previous studies indicated CIP4-CaNAβ2 signalosomes inhibit pathological cardiac hypertrophy.

    Purpose of the Study:

    • To investigate the role of CIP4-CaNAβ2 signalosomes in cardioprotection and cardiac remodeling following ischemic heart disease.
    • To evaluate the therapeutic potential of targeting CIP4-CaNAβ2 interactions in mouse models of myocardial infarction and chronic ischemic cardiomyopathy.

    Main Methods:

    • Utilized CIP4 conditional knock-out (CKO) mice and adeno-associated virus (AAV)-mediated gene transfer in wildtype mice.
    • Assessed cardiac function and infarct size using echocardiography, strain analysis, and histology after ischemia-reperfusion (I/R) injury and permanent left coronary artery (LCA) ligation.
    • Investigated the effects of inhibiting CaNAβ2 expression, CaN-NFAT signaling (VIVIT peptide), or CIP4-CaNAβ2 binding (PP peptide) in cardiomyocytes and T-cells.

    Main Results:

    • CIP4 CKO mice and mice expressing the PP peptide showed preserved cardiac function and reduced infarct size after I/R injury and myocardial infarction.
    • Cardiomyocyte-specific depletion of CaNAβ2 or VIVIT peptide worsened outcomes in I/R injury and chronic ischemic cardiomyopathy models.
    • PP-mediated inhibition of CaNAβ anchoring did not affect T-cell activation or cytokine expression in vitro.

    Conclusions:

    • CIP4-CaNAβ2 signalosomes promote adverse cardiac remodeling and are not cardioprotective in ischemic heart disease.
    • Targeting CIP4-CaNAβ2 complexes offers a potential therapeutic strategy for cardiovascular diseases, including ischemic cardiomyopathy and myocardial infarction.
    • Gene therapy with a PP anchoring disruptor peptide provides proof-of-concept for treating acute and chronic ischemic heart conditions.