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Cardiomyocyte death: mechanisms and translational implications

Cell Death and Disease · 2011 · Vol. 2(12) · pp. e244–e244
Mario ChiongZhao WangZully PedrozoDian J. CaoRodrigo TroncosoMauricio IbacacheAlfredo CriolloAndriy NemchenkoJoseph A. HillSergio Lavandero

Abstract

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.

Autophagy in Disease and TherapyCell death mechanisms and regulationCalpain Protease Function and RegulationAutophagyNecrosisApoptosisMyocardial infarctionProgrammed cell deathMedicineCardiac myocyteDiseaseCause of deathIschemia

MeSH terms

AutophagyCardiovascular DiseasesHumansMitochondriaNecrosisProtein BiosynthesisApoptosisMyocytes, CardiacStem Cell Transplantation

Funding

  • American Heart Association
  • National Institutes of Health
  • Fondo de Financiamiento de Centros de Investigación en Áreas Prioritarias
Citations
484
FWCI
11.38
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