title: The role of apoptotic cell death in cardiovascular disease.
abstract: BACKGROUND
  Programmed cell death, or apoptosis, is a distinct, managed form of cell death. It is fundamentally different from necrosis. It is a genetically controlled, energy-dependent method of cellular deletion without inflammation. In the cardiovascular system, apoptosis occurs as a primary and secondary event in disease pathogenesis. This review addresses our current understanding of the initiation, propagation and significance of apoptosis in the cardiovascular system, as well as assessing therapeutic potentials arising therefrom.
  
  
  METHODS
  A Medline search was performed and relevant publications reviewed. Further articles were obtained from the references of these publications.
  
  
  RESULTS
  and conclusions Apoptotic cell death is a key element in the pathogenesis and progression of ischaemia-reperfusion (IR) injury, cardiac failure, myocardial infarction, atherosclerosis, endothelial dysfunction and the clinical syndromes which these situations produce. Our increased understanding of the role of apoptosis in the pathogenesis of cardiovascular disease offers potential to develop new therapeutic strategies.
authors.affiliation: Department of Surgery, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
authors.forename: R
authors.initials: R
authors.lastname: McLaughlin
authors.forename: C J
authors.initials: CJ
authors.lastname: Kelly
authors.forename: E
authors.initials: E
authors.lastname: Kay
authors.forename: D
authors.initials: D
authors.lastname: Bouchier-Hayes
mesh_terms: D017209:Apoptosis / Q000235:genetics / Q000502:physiology*; D001161:Arteriosclerosis / Q000503:physiopathology; D009202:Cardiomyopathies / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000473:pathology / Q000503:physiopathology*; D002319:Cardiovascular System / Q000473:pathology; D020169:Caspases / Q000502:physiology; D006801:Humans; D006965:Hyperplasia / Q000473:pathology / Q000503:physiopathology; D009569:Nitric Oxide / Q000502:physiology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology; D015427:Reperfusion Injury / Q000503:physiopathology; D017539:Tunica Intima / Q000473:pathology / Q000503:physiopathology
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D009569:Nitric Oxide; D020169:Caspases