Bcl-2 protein family: implications in vascular apoptosis and atherosclerosis.
Apoptosis has been recognized as a central component in the pathogenesis of atherosclerosis, in addition to the other human pathologies such as cancer and diabetes. The pathophysiology of atherosclerosis is complex, involving both apoptosis and proliferation at different phases of its progression. Oxidative modification of lipids and inflammation differentially regulate the apoptotic and proliferative responses of vascular cells during progression of the atherosclerotic lesion. Bcl-2 proteins act as the major regulators of extrinsic and intrinsic apoptosis signalling pathways and more recently it has become evident that they mediate the apoptotic response of vascular cells in response to oxidation and inflammation either in a provocative or an inhibitory mode of action. Here we address Bcl-2 proteins as major therapeutic targets for the treatment of atherosclerosis and underscore the need for the novel preventive and therapeutic interventions against atherosclerosis, which should be designed in the light of molecular mechanisms regulating apoptosis of vascular cells in atherosclerotic lesions.
Kutuk
Ozgur
O
Biological Sciences and Bioengineering Program, Faculty of Engineering and Natural Sciences, Sabanci University, 34956 Orhanli, Tuzla, Istanbul, Turkey.
Basaga
Huveyda
H
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001161:Arteriosclerosis / Q000209:etiology* / Q000378:metabolism; D004249:DNA Damage / Q000502:physiology; D006801:Humans; D008928:Mitochondria / Q000502:physiology; D008954:Models, Biological; D005810:Multigene Family / Q000502:physiology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology*; D015398:Signal Transduction; D014652:Vascular Diseases / Q000209:etiology / Q000378:metabolism
D019253:Proto-Oncogene Proteins c-bcl-2