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Chemerin in atherosclerosis
Jia-Xiang Sun1, Chi Zhang2, Zhe-Bin Cheng3
1Research Laboratory of Translational Medicine, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China; Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China; Departments of Clinical Medicine, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China.
Chemerin, an adipokine, plays complex roles in atherosclerosis (AS) pathogenesis, influencing inflammation and cell proliferation. Further research is needed to clarify its dual effects and develop targeted therapies for this arterial disease.
Area of Science:
- Cardiovascular Science
- Endocrinology
- Inflammation Research
Background:
- Atherosclerosis (AS) involves endothelial dysfunction, inflammation, and lipid accumulation.
- Adipokines, secreted by adipose tissue, are increasingly linked to cardiovascular diseases like AS.
- Chemerin, an adipokine, is associated with inflammation, metabolic disorders, and vascular cell abnormalities relevant to AS.
Purpose of the Study:
- To review the role of chemerin and its receptors in the pathogenesis of atherosclerosis.
- To synthesize current understanding of chemerin's contradictory effects in AS.
- To identify knowledge gaps and suggest future research directions for chemerin in AS.
Main Methods:
- Literature review of studies on chemerin and atherosclerosis.
- Analysis of existing data on chemerin's association with inflammation, endothelial function, and VSMC proliferation.
- Synthesis of evidence regarding chemerin's anti- and pro-atherogenic effects.
Main Results:
- Chemerin exhibits diverse and sometimes conflicting roles in AS, including effects on vascular calcification and endothelial function.
- Its atherogenic or anti-atherogenic impact appears context-dependent and cell-specific.
- Current data highlight significant gaps in understanding chemerin's precise role in AS etiology.
Conclusions:
- Chemerin's multifaceted role in AS pathogenesis requires further investigation.
- Targeted chemerin-based therapies hold potential for innovative AS treatment strategies.
- Future studies should focus on elucidating chemerin's specific functions in different cellular contexts within AS.
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