Nitric oxide and promotion of cardiac myocyte apoptosis

Péter Andréka, Thanh Tran, Keith A. Webster, Nanette H. Bishopric

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

The removal of damaged, superfluous or energy-starved cells is essential for biological homeostasis, and occurs in every tissue type. Programmed cell death occurs through several closely regulated signal pathways, including apoptosis, in which cell components are broken down and packaged into small membrane-bound fragments that are then removed by neighbouring cells or phagocytes. This process is activated in the cardiac myocyte in response to a variety of stresses, including oxidative and nitrosative stress, and involves mitochondria-derived signals. Loss of cardiac myocytes through apoptosis has been shown to induce cardiomyopathy in a variety of gene-targeted animal models. Because cardiac myocytes have strictly limited ability to regenerate, sustained programmed cell death is likely to contribute to the development and progression of heart failure in a variety of myocardial diseases. At the same time, the cardiac myocyte possesses a number of mechanisms for defence against short-term haemodynamic and oxidative stresses. Our laboratory has recently examined the role of nitric oxide (NO) as a regulator of the programmed death of cardiac myocytes, and the potential contribution of NO and NO-dependent signalling to the loss of myocytes in heart failure. We will review the role of c-Jun N-terminal kinase in response to oxidative and nitrosative stress, and summarise evidence for its role as a cytoprotective mechanism. We will also review evidence implicating NO in the pathophysiology of heart failure, in the context of the extensive and sometimes contradictory body of research on NO and cell survival.

Original languageEnglish (US)
Pages (from-to)35-53
Number of pages19
JournalMolecular and Cellular Biochemistry
Volume263
Issue number1
DOIs
StatePublished - Aug 2004

Keywords

  • Apoptosis
  • Bcl-2-related proteins
  • Bnip-3
  • c-Jun N-terminal kinase
  • Cardiac myocyte
  • Caspases
  • Heart failure
  • Mitochondria
  • Nitric oxide
  • Oxidative stress
  • Peroxynitrite
  • Programmed cell death

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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