[Death by apoptosis of cardiomyocytes: from the cells to clinics].
Cell hypertrophy, modulations of gene expression or changes of the activity of proteins are known to play a role in remodelling of diseased myocardium. However, few data are available concerning regulation of the cell mass in heart disease. While cardiomyocyte hyperplasia remains controversial and probably constitutes a negligible phenomenon, the decreased number of cells could arguably contribute to alterations of the pathological myocardium. This loss of myocytes was mainly attributed to process of cell necrosis until it was demonstrated that cardiac myocytes can also die via apoptosis. This has been observed in ischaemic [1], hypertrophic [2], and dilated [3, 4] cardiomyopathy and in arrhythmogenic right ventricular dysplasia [5], to mention only the main diseases, and this list continues to grow [6]. Apoptosis therefore constitutes a major biological phenomenon in cardiology, at least at congresses and in scientific publications, but its place and significance in the pathophysiology of heart disease has yet to be established.
Hatem
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INSERM Unité 460, Faculté de Médecine Xavier Bichat, Paris.
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D009202:Cardiomyopathies / Q000473:pathology* / Q000503:physiopathology; D006321:Heart / Q000503:physiopathology; D006801:Humans; D009206:Myocardium / Q000166:cytology / Q000473:pathology*
Mort par apoptose des myocytes cardiaques: de la cellule à la clinique.