Cell death in the myocardium: My heart won't go on

DOI Web Site Web Site 被引用文献2件
  • Amabel M. Orogo
    Skaggs School of Pharmacy and Pharmaceutical Sciences Department of Pharmacology, University of California San Diego, La Jolla CA USA
  • Åsa B. Gustafsson
    Skaggs School of Pharmacy and Pharmaceutical Sciences Department of Pharmacology, University of California San Diego, La Jolla CA USA

書誌事項

公開日
2013-07-03
権利情報
  • http://onlinelibrary.wiley.com/termsAndConditions#vor
DOI
  • 10.1002/iub.1180
公開者
Wiley

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説明

<jats:title>Abstract</jats:title><jats:p>Loss of cardiomyocytes plays a critical role in the pathogenesis of heart failure. With fewer myocytes, the heart is unable to sustain efficient contraction. Much attention has been focused on understanding mechanisms of cell death in myocytes with the ultimate goal being to reduce the extent of injury and improve function in the failing myocardium. Both necrosis and apoptosis contribute to loss of myocytes, and this loss of cells is a hallmark of cardiac pathologies, including ischemia/reperfusion, myocardial infarction, and heart failure. Apoptosis is a highly regulated process that is activated via death receptors in the plasma membrane or via permeabilization of the mitochondria. Necrosis is generally viewed as an uncontrolled process that leads to mitochondrial swelling, cell rupture, and subsequent inflammation. However, recent studies have uncovered a signaling pathway that mediates regulated necrosis or necroptosis. Mitochondria play an important role in both apoptosis and necrosis, and changes in their morphology can affect the cells' susceptibility to stress. This review focuses on the various modes of cell death in the myocardium and highlights how they contribute to loss of myocytes in response to stress. © 2013 IUBMB Life, 65(8):651–656, 2013</jats:p>

収録刊行物

  • IUBMB Life

    IUBMB Life 65 (8), 651-656, 2013-07-03

    Wiley

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