Apoptosis in heart failure represents programmed cell survival, not death, of cardiomyocytes and likelihood of reverse remodeling

Nezam Haider, Navneet Narula, Jagat Narula

Research output: Contribution to journalArticlepeer-review

50 Scopus citations

Abstract

Apoptosis is a highly orchestrated form of programmed cell death, and this is believed to contribute to continuous decline of ventricular function in heart failure. However, the apoptotic cascade is not completed in failing myocardium and DNA damage is prevented due to abolition of DNA fragmentation factors. The extranuclear apoptotic program is interrupted secondary to inhibition of activated caspase-3 by upregulated inhibitors of apoptotic process. During the apoptotic process, upstream step comprising extensive mitochondrial loss of cytochrome c may contribute to systolic dysfunction of heart. Intactness of nuclear blueprint underscores the likelihood of reverse remodeling that has been demonstrated in the post-LVAD myocardial specimens.

Original languageEnglish
Pages (from-to)S512-S517
JournalJournal of Cardiac Failure
Volume8
Issue number6 SUPPL.
DOIs
StatePublished - Dec 2002
Externally publishedYes

Keywords

  • Apoptosis interruptus
  • Nerosis
  • Remodeling caspases
  • Zombie myocytes

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