Objective： To review the functional mechanism of apolipoprotein J （apoJ） in the process of atherosclerosis and the feasibility of apoJ as a therapeutic endpoint. Data Sources： Relevant articles published in Englis...Objective： To review the functional mechanism of apolipoprotein J （apoJ） in the process of atherosclerosis and the feasibility of apoJ as a therapeutic endpoint. Data Sources： Relevant articles published in English from 1983 to present were selected from PubMed. The terms of＂atherosclerosis. apolipoprotein J, clusterin （CLU）, oxidative stress, and inflammation＂ were used for searching. Study Selection： Articles studying the role ofapoJ with atherosclerosis and restenosis after injury were reviewed. Articles focusing on the intrinsic determinants of atherosclerosis were selected. The exclusion criteria of articles were that the studies on immunologic vasculitis. Results： ApoJ, involved in numerous physiological process important for lipid transportation and vascular smooth muscle cell differentiation, including apoptotic cell death, cell-cycle regulation, cell adhesion, tissue remodeling, immune system regulation, and oxidative stress, plays a role in the development of clinical atherosclerosis. In the process of relieving atherosclerosis, apoJ can promote cholesterol and phospholipid export from macrophage-foam cells, and exhibit cytoprotective and anti-inflammatory actions by interacting with lots of known inflammatory proteins which may predict the onset of clinical cardiovascular events and may actually play a causal role in mediating atherosclerotic disease such as C-reactive protein, paraoxonase, and leptin. As known as CLU, apoJ has been identified to play central roles in the process of vascular smooth cells migration, adhesion, and proliferation, which can contribute significantly to restenosis atter vascular injury. Conclusions： Intense effort and substantial progress have been made to identify the apoJ that relieves atherosclerosis and vascular restenosis after percutaneous coronary intervention. More work is needed to elucidate the exact mechanisms of and the interrelationship between the actions ofapoJ and to successfully achieve regression ofatherosclerosis by regarding it as a therapeutic endpoint.展开更多
基金a grant of the Key Technology and Science Foundation of Tianjin,China
文摘Objective： To review the functional mechanism of apolipoprotein J （apoJ） in the process of atherosclerosis and the feasibility of apoJ as a therapeutic endpoint. Data Sources： Relevant articles published in English from 1983 to present were selected from PubMed. The terms of＂atherosclerosis. apolipoprotein J, clusterin （CLU）, oxidative stress, and inflammation＂ were used for searching. Study Selection： Articles studying the role ofapoJ with atherosclerosis and restenosis after injury were reviewed. Articles focusing on the intrinsic determinants of atherosclerosis were selected. The exclusion criteria of articles were that the studies on immunologic vasculitis. Results： ApoJ, involved in numerous physiological process important for lipid transportation and vascular smooth muscle cell differentiation, including apoptotic cell death, cell-cycle regulation, cell adhesion, tissue remodeling, immune system regulation, and oxidative stress, plays a role in the development of clinical atherosclerosis. In the process of relieving atherosclerosis, apoJ can promote cholesterol and phospholipid export from macrophage-foam cells, and exhibit cytoprotective and anti-inflammatory actions by interacting with lots of known inflammatory proteins which may predict the onset of clinical cardiovascular events and may actually play a causal role in mediating atherosclerotic disease such as C-reactive protein, paraoxonase, and leptin. As known as CLU, apoJ has been identified to play central roles in the process of vascular smooth cells migration, adhesion, and proliferation, which can contribute significantly to restenosis atter vascular injury. Conclusions： Intense effort and substantial progress have been made to identify the apoJ that relieves atherosclerosis and vascular restenosis after percutaneous coronary intervention. More work is needed to elucidate the exact mechanisms of and the interrelationship between the actions ofapoJ and to successfully achieve regression ofatherosclerosis by regarding it as a therapeutic endpoint.
