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Apolipoprotein J: A New Predictor and Therapeutic Target in Cardiovascular Disease?
Insights
Apolipoprotein J (apoJ) plays a key role in atherosclerosis by regulating lipid transport and inflammation. Further research is needed to fully understand apoJ
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Atherosclerosis is a complex vascular disease involving lipid accumulation, inflammation, and cellular dysfunction.
- Apolipoprotein J (apoJ), also known as clusterin (CLU), is a multifunctional protein implicated in various physiological and pathological processes.
- Understanding the precise role of apoJ in atherosclerosis is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To review the functional mechanisms of apolipoprotein J (apoJ) in the development of atherosclerosis.
- To assess the potential of apoJ as a therapeutic target or endpoint for atherosclerosis and restenosis.
Main Methods:
- A comprehensive literature search was conducted using PubMed, covering articles from 1983 to the present.
- Keywords included "atherosclerosis, apolipoprotein J, clusterin (CLU), oxidative stress, and inflammation."
- Studies focusing on apoJ's role in atherosclerosis and restenosis after vascular injury were selected, excluding immunologic vasculitis research.
Main Results:
- ApoJ is involved in lipid transport, vascular smooth muscle cell differentiation, apoptosis, cell-cycle regulation, and oxidative stress, contributing to atherosclerosis.
- ApoJ promotes cholesterol and phospholipid export from foam cells and exhibits cytoprotective and anti-inflammatory effects.
- ApoJ (CLU) plays a significant role in vascular smooth cell migration, adhesion, and proliferation, impacting restenosis post-injury.
Conclusions:
- Significant progress has been made in identifying apoJ's role in mitigating atherosclerosis and vascular restenosis.
- Further investigation is required to elucidate the exact mechanisms and interrelationships of apoJ's actions.
- ApoJ holds promise as a potential therapeutic endpoint for achieving atherosclerosis regression.
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 of apoJ 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 after 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 of apoJ and to successfully achieve regression of atherosclerosis by regarding it as a therapeutic endpoint.
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