Myocyte apoptosis in heart failure

Cardiovasc Res. 2005 Jul 1;67(1):21-9. doi: 10.1016/j.cardiores.2005.04.012.

Abstract

Human heart failure is preceded by a process termed cardiac remodeling in which heart chambers progressively enlarge and contractile function deteriorates. Programmed cell death (apoptosis) of cardiac muscle cells has been identified as an essential process in the progression to heart failure. The execution of the apoptotic program entails complex interactions between and execution of multiple molecular subprograms. Unlike necrosis, apoptosis is an orderly regulated process and, by inference, a logical therapeutic target if intervention occurs at an early stage. To identify potential therapeutic targets, it is imperative to have a full understanding of the apoptotic pathways that are functional in the cardiac muscle. Accordingly, the present review summarizes the apoptotic pathways operative in cardiac muscle and discusses therapeutic options related to apoptosis for the future treatment of human heart failure.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Caspases / metabolism
  • Heart Failure / metabolism
  • Heart Failure / pathology*
  • Humans
  • Ion Channels
  • Mitochondrial Membrane Transport Proteins
  • Mitochondrial Permeability Transition Pore
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology*
  • Receptors, Tumor Necrosis Factor / metabolism
  • Signal Transduction / physiology
  • Ventricular Remodeling*
  • fas Receptor / metabolism

Substances

  • Ion Channels
  • Mitochondrial Membrane Transport Proteins
  • Mitochondrial Permeability Transition Pore
  • Receptors, Tumor Necrosis Factor
  • fas Receptor
  • Caspases