To die or not to die: an overview of apoptosis and its role in disease

JAMA. 1998 Jan 28;279(4):300-7. doi: 10.1001/jama.279.4.300.


The death of cells in tissues of humans and other multicellular organisms is neither always abnormal nor always detrimental. Although necrosis ensues at the sites of massive cellular injury, most cells in the body die through a more subtle, noninflammatory, energy-dependent form of cell death called apoptosis. The number of cells in tissues is determined by the homeostatic balance between proliferation of new cells and death of senescent cells; the rates of proliferation and apoptosis vary widely from tissue to tissue. Recent research into the molecular mechanisms of apoptosis has revealed that apoptosis is a genetically programmed process that can become deranged when the components of the cellular apoptotic machinery are mutated or present in inappropriate quantities. Dysregulation of apoptosis is associated with the pathogenesis of a wide array of diseases: cancer, neurodegeneration, autoimmunity, heart disease, and other disorders. Products of genes involved in the regulation and execution of apoptosis are potentially excellent targets for diagnosis and therapeutic intervention in disease processes, and they offer renewed hope for cures and treatments for a wide array of maladies.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis* / genetics
  • Apoptosis* / physiology
  • Apoptotic Protease-Activating Factor 1
  • Autoimmune Diseases
  • Autoimmunity
  • Caenorhabditis elegans
  • Cysteine Endopeptidases / physiology
  • Genes, bcl-2 / physiology
  • Graft Rejection
  • Heart Diseases
  • Humans
  • Ligands
  • Lymphoproliferative Disorders
  • Mitochondria / physiology
  • Neurodegenerative Diseases
  • Proteins / physiology
  • Receptors, Cell Surface / physiology
  • T-Lymphocytes / physiology


  • APAF1 protein, human
  • Apoptotic Protease-Activating Factor 1
  • Ligands
  • Proteins
  • Receptors, Cell Surface
  • Cysteine Endopeptidases