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Cardiomyocyte death: mechanisms and translational implications

Journal

CELL DEATH & DISEASE
Volume 2, Issue -, Pages -

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/cddis.2011.130

Keywords

apoptosis; autophagy; cardiovascular diseases; heart; necrosis

Categories

Funding

  1. NIH [HL-075173, HL-080144, HL-090842]
  2. AHA [0640084N, 10POST4320009]
  3. AHA-Jon Holden DeHaan Foundation [0970518N]
  4. Fondo Nacional de Desarrollo Cientifico y Tecnologico [FONDECYT 1080436, FONDAP 15010006]
  5. FONDECYT [3110039, 3110114]

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Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Although treatments have improved, development of novel therapies for patients with CVD remains a major research goal. Apoptosis, necrosis, and autophagy occur in cardiac myocytes, and both gradual and acute cell death are hallmarks of cardiac pathology, including heart failure, myocardial infarction, and ischemia/reperfusion. Pharmacological and genetic inhibition of autophagy, apoptosis, or necrosis diminishes infarct size and improves cardiac function in these disorders. Here, we review recent progress in the fields of autophagy, apoptosis, and necrosis. In addition, we highlight the involvement of these mechanisms in cardiac pathology and discuss potential translational implications. Cell Death and Disease (2011) 2, e244; doi:10.1038/cddis.2011.130; published online 22 December 2011

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