血管平滑肌细胞──祸首还是福星

Vascular Smooth Miscle Cell : Culprit or Mascot in Atherosclerotic Disease

长期以来血管平滑肌细胞（ＶＳＭＣ）增殖被认为是动脉粥样硬化（ＡＳ）发生的绝对必要条件和介入性治疗后血管再狭窄（ＲＳ）的主要原因。许多抗ＡＳ和ＲＳ的策略始终盯住抑制ＶＳＭＣ增殖这一环节。然而这些方法在临床试验中很少见到或基本没有益处（尤其是对ＲＳ）。近来的临床和实验研究提示抑制ＶＳＭＣ可以导致脆弱的ＡＳ斑块不稳定而发生裂缝、破裂、血栓形成，引起心肌梗死等急性冠状动脉症候群，因为ＶＳＭＣ合成释放的胶原等可以增加斑块的生物力学强度。如今，缺血性心脏病已不再被认为是粥样硬化病灶中的胆固醇、钙和纤维组织等积聚起来机械性地阻塞血流所致。容易破裂的斑块中平滑肌细胞数减少，且这种斑块并不常常引起限制血流的狭窄的事实警示我们有必要辩证地看待ＶＳＭＣ增殖在动脉粥样硬化性疾病中的利与弊，并以新的角度审视在预防和治疗这类疾病的研究及临床实践中所采取的有关对策。

Proliferation of vascular smooth muscle cells has been considered the sine qua non of,and held center stageas the culprit in atherosclerotic disease for several decardes. Many strategies for combating atherosclerosis and restenosistarget smooth muscle replication. However, few or none (especially for restenosis) have proven beneficial in clinical trials.Furthermore,recent clinical and experimental evidence suggests that inbitition of smooth muscle proliferation in patientsmight produce the undesired effect of destabilizing vulnerable atherosclerotic plaques because these cells furnish the collagenresponsible for the biomechanical strength of plaque. No longer is ischemic heart disease thonght of as a mechanicalblockage caused by the progressive accumulation of cholesteral, celcium, and fibrous tissue in an atheroma. The fact thatplaques vulnerable to disruption often do not produce flow - limiting stenoses hightights a need for assessing the beneficialeffect of smooth muscle cell proliferation mliferation in atherosclerosis and reassessing the strategies to treat or prevent the acute coronary syndromes.