• Cellular and molecular approaches to enhance myocardial recovery after myocardial infarction

    Highlights

    • Infarct size is a major determinant of prognosis after myocardial infarction.
    • Various therapies have successfully reduced infarct size in animal models, but not in humans.
    • We review ongoing studies and future strategies to reduce infarct size after large myocardial infarction.

    Abstract

    Reperfusion therapy has resulted in significant improvement in post-myocardial infarction morbidity and mortality in over the last 4 decades. Nonetheless, it is well recognized that simply restoring patency of the epicardial artery may not stop or reverse damage at microvascular level, and myocardial salvage is often suboptimal. Numerous efforts have been undertaken to elucidate the mechanisms underlying extensive myonecrosis to facilitate the discovery of therapies to provide additional and incremental benefits over current therapeutic pathways. To date, conclusively effective strategies to promote myocardial recovery have not yet been established. Novel approaches are investigating the foundational cellular and molecular bases of myocardial ischemia and irreversible injury. Herein, we review the emerging concepts and proposed therapies that may improve myocardial protection and reduce infarct size. We examine the preclinical and clinical evidence for reduced infarct size with these strategies, including anti-inflammatory agents, intracellular ion channel modulators, agents affecting the reperfusion injury salvage kinase (RISK) and nitric oxide signaling pathways, modulators of mitochondrial function, anti-apoptoticagents, and stem cell and gene therapy. We review the potential reasons of failures to date and the potential for new strategies to further promote myocardial recovery and improve prognosis.

    Author bio

    Cardiovascular Revascularization Medicine, 2019-04-01, Volume 20, Issue 4, Pages 351-364, Copyright © 2018 Elsevier Inc.

     

    Source:

    Read the full article on Science Direct: Cellular and molecular approaches to enhance myocardial recovery after myocardial infarction

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