Oxidized LDL-Induced injury and apoptosis in atherosclerosis - Potential roles for oxysterols

被引:161
作者
Colles, SM
Maxson, JM
Carlson, SG
Chisolm, GM
机构
[1] Cleveland Clin Fdn, Lerner Res Inst, Dept Cell Biol, Cleveland, OH 44195 USA
[2] Cleveland Clin Fdn, Lerner Res Inst, Dept Biomed Engn, Cleveland, OH 44195 USA
关键词
D O I
10.1016/S1050-1738(01)00106-2
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
The cell injury caused by oxidized lipoproteins was among the first findings that led to the theory that it is the oxidation of low-density lipoprotein (LDL), not just LDL concentration, that leads to arterial disease. Voluminous studies have now revealed that oxidized lipoproteins and their constituents can induce numerous effects on cells that can be construed to be atherogenic. Cell injury is but one of these, and it is these injurious effects that are the focus of this brief review. Cell injury and death appear to play multiple roles in lesion development and the toxic lipid constituents of oxidized lipoproteins, including a variety of oxysterols, are candidates for the in vivo effectors of this cytotoxicity. Recent studies have focused on the mechanisms of oxidized lipoprotein-induced cell death, whether the cells die by apoptosis or necrosis, and the identities of the toxins that induce injury. Understanding the roles of these agents in lesion development could lead to therapies that modulate cell death and inhibit lesion formation. (C) 2001, Elsevier Science Inc.
引用
收藏
页码:131 / 138
页数:8
相关论文
共 107 条
[1]
ALI S, 1993, J BIOL CHEM, V268, P17397
[2]
7β-hydroxycholesterol induces Ca2+ oscillations, MAP kinase activation and apoptosis in human aortic smooth muscle cells [J].
Ares, MPS ;
Pörn-Ares, MI ;
Moses, S ;
Thyberg, J ;
Juntti-Berggren, L ;
Berggren, PO ;
Hultgårdh-Nilsson, A ;
Kallin, B ;
Nilsson, J .
ATHEROSCLEROSIS, 2000, 153 (01) :23-35
[3]
Ares MPS, 1997, J LIPID RES, V38, P2049
[4]
Sphingomyelin metabolites in vascular cell signaling and atherogenesis [J].
Augé, N ;
Nègre-Salvayre, A ;
Salvayre, R ;
Levade, T .
PROGRESS IN LIPID RESEARCH, 2000, 39 (03) :207-229
[5]
BALL RY, 1987, ARCH PATHOL LAB MED, V111, P1134
[6]
MINIMALLY MODIFIED LOW-DENSITY-LIPOPROTEIN STIMULATES MONOCYTE ENDOTHELIAL INTERACTIONS [J].
BERLINER, JA ;
TERRITO, MC ;
SEVANIAN, A ;
RAMIN, S ;
KIM, JA ;
BAMSHAD, B ;
ESTERSON, M ;
FOGELMAN, AM .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 85 (04) :1260-1266
[7]
Receptors for oxidized low-density lipoprotein on elicited mouse peritoneal macrophages can recognize both the modified lipid moieties and the modified protein moieties:: Implications with respect to macrophage recognition of apoptotic cells [J].
Bird, DA ;
Gillotte, KL ;
Hörkkö, S ;
Friedman, P ;
Dennis, EA ;
Witztum, JL ;
Steinberg, D .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (11) :6347-6352
[8]
Overexpression of PHGPx inhibits hydroperoxide-induced oxidation, NFκB activation and apoptosis and affects oxLDL-mediated proliferation of rabbit aortic smooth muscle cells [J].
Brigelius-Flohé, R ;
Maurer, S ;
Lötzer, K ;
Böl, GF ;
Kallionpää, H ;
Lehtolainen, P ;
Viita, H ;
Ylä-Herttuala, S .
ATHEROSCLEROSIS, 2000, 152 (02) :307-316
[9]
Oxysterols and atherosclerosis [J].
Brown, AJ ;
Jessup, W .
ATHEROSCLEROSIS, 1999, 142 (01) :1-28
[10]
Brown AJ, 1997, J LIPID RES, V38, P1730