Cell suicide and caspases

Vascul Pharmacol. 2007 Jun;46(6):383-93. doi: 10.1016/j.vph.2007.01.006. Epub 2007 Feb 8.


Programmed cell death or apoptosis is a well regulated physiological form of cellular autodestruction. It plays an essential role in embryonic development, homeostasis, remodeling, surveillance, and host defense mechanisms. Conversely dysregulation of apoptosis, resulting in either too less or excessive cell death is implicated in pathogenesis of stroke, myocardial infarction, neurodegenerative diseases, cancer and autoimmmune disorders. Apoptosis is coordinated by a family of cysteine proteinases called caspases, which dismantle the cell by targeting panoply of proteins. The mammalian caspase family contains 14 members, a subset participates in cellular demise and the remaining are involved in the processing of pro-inflammatory cytokines. We have tried to develop a simplified picture of basic apoptotic mechanisms on the basis of recent insights into the area.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis* / drug effects
  • Caspase Inhibitors
  • Caspases / metabolism*
  • Cysteine Proteinase Inhibitors / metabolism
  • Cysteine Proteinase Inhibitors / pharmacology
  • Enzyme Activation
  • Humans
  • Isoenzymes / metabolism
  • Mitochondria / metabolism
  • Myocardial Reperfusion Injury / metabolism
  • Myocardial Reperfusion Injury / pathology
  • Receptors, Death Domain / metabolism
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology
  • Signal Transduction* / drug effects


  • Caspase Inhibitors
  • Cysteine Proteinase Inhibitors
  • Isoenzymes
  • Receptors, Death Domain
  • Caspases