Rössig L, Dimmeler S, Zeiher A M
Department of Medicine IV, University of Frankfurt, Germany.
Basic Res Cardiol. 2001 Feb;96(1):11-22. doi: 10.1007/s003950170073.
Apoptosis, programmed cell death, has emerged as a key element in the complex pathophysiology underlying the development as well as the progression of atherosclerosis. A number of recent reports provided evidence for both in vivo and in vitro occurrence of apoptotic cell death of vascular cells, namely endothelial cells, macrophages, and vascular smooth muscle cells. In addition, functional studies in disease models underscore the relevance of these findings for the understanding of processes which lead to lesion development, plaque rupture, and thrombus formation. Pathomechanistic in vitro investigations provided an increasingly detailed picture of the involved intracellular signaling pathways that regulate onset and execution of apoptosis. These insights offer the potential of therapeutic interventions targeted to interfere with the molecular processes involving apoptotic cell death in the vascular wall.
细胞凋亡，即程序性细胞死亡，已成为动脉粥样硬化发生和发展的复杂病理生理学中的关键因素。最近的一些报告提供了体内和体外血管细胞（即内皮细胞、巨噬细胞和血管平滑肌细胞）发生凋亡性细胞死亡的证据。此外，疾病模型中的功能研究强调了这些发现对于理解导致病变发展、斑块破裂和血栓形成过程的相关性。体外病理机制研究对调节细胞凋亡起始和执行的相关细胞内信号通路提供了越来越详细的描述。这些见解为针对干扰血管壁中涉及凋亡性细胞死亡的分子过程的治疗干预提供了潜力。
