In atherogenesis, the apoptosis of endothelial cell itself could directly induce over-proliferation of smooth muscle cells.
Over-proliferation of SMC (smooth muscle cell) is one characteristics of atherosclerosis. One well accepted mechanism is that the decrease of ECs (endothelial cells) induced by over apoptosis leads to endothelial dysfunction, which in turn results in over-proliferation of SMC. Obviously, the mechanism works after endothelial apoptosis. Compared with necrosis, apoptosis is time and energy consuming. The question is why the cell ends in the form of apoptosis instead of necrosis. From the evolutionary standpoint, apoptosis has some useful functions other than removing the damaged or unwanted cells. Recent studies showed that cells nearby the apoptotic ones began to proliferate and differentiate before apoptosis and the apoptotic signals could induce the near cells to proliferate without the death of cells. Apparently, some mechanism in apoptosis results in the proliferation of cells. So, we hypotheses that endothelial apoptosis can directly induce the over-proliferation of SMC.
Qin
Chunchang
C
Centre of pulmonary vascular disease, Fuwai Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 10037, China.
Liu
Zhihong
Z
D017209:Apoptosis; D050197:Atherosclerosis / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D002455:Cell Division; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000473:pathology*
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors