Molecular signal transduction in vascular cell apoptosis  

作　　者：GENG YONG JIAN Center for Cardiovascular Biology and Atherosclerosis Research, Division of Cardiology, Department of Internal Medicine, University of Texas Houston Health Science Center Medical School, 6431 Fannin Street, MSB 6.045, Houston, TX 77030, USA 

出　　处：《Cell Research》2001年第4期253-264,共12页细胞研究（英文版）

摘　　要：Apoptosis is a form of genetically programmed cell death, which plays a key role in regulation of cellularity in a variety of tissue and cell types including the cardiovascular tissues. Under both physiological and pathophysiological conditions, various biophysiological and biochemical factors, including mechanical forces, reactive oxygen and nitrogen species, cytokines, growth factors, oxidized lipoproteins, etc., may influence apoptosis of vascular cells. The Fas/Fas ligand/caspase death-signaling pathway, Bcl-2 protein family/mitochondria, the tumor suppressive gene p53, and the proto-oncogene c-myc may be activated in atherosclerotic lesions, and mediates vascular apoptosis during the development of atherosclerosis. Abnormal expression and dysfunction of these apoptosis-regulating genes may attenuate or accelerate vascular cell apoptosis and affect the integrity and stability of atherosclerotic plaques. Clarification of the molecular mechanism that regulates apoptosis may help design a new strategy for treatment of atherosclerosis and its major complication, the acute vascular syndromes.

关 键 词：Apoptosis Signal Transduction ARTERIOSCLEROSIS Comparative Study Endothelium  Vascular Humans Models  Biological Muscle  Smooth  Vascular Research Support  U.S. Gov't  P.H.S. 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学]