A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages

被引：7
|
作者：
Hu, Jiaxin [1 ]
Zhang, Ying [1 ]
Hu, Liaoping [1 ]
Chen, Haiting [1 ]
Wu, Han [1 ]
Chen, Jianzhou [1 ]
Xie, Jun [1 ]
Xu, Biao [1 ]
Wei, Zhonghai [1 ]
机构：
[1] Nanjing Univ, Med Sch, Affiliated Hosp,Nanjing Drum Tower Hosp, Dept Cardiol,MOE Key Lab Model Anim Dis Study Nan, Nanjing 210061, Peoples R China
来源：
JOURNAL OF TRANSLATIONAL MEDICINE | 2022年 / 20卷 / 01期
关键词：
Syndecan-4; Atherosclerosis; Macrophage; Ox-LDL; ApoE(-/-); NEUTROPHIL MIGRATION; CHOLESTEROL EFFLUX; INFLAMMATION; CELLS; HDL; EXPRESSION; DISEASE; TARGETS; ABCA1;
D O I：
10.1186/s12967-022-03505-5
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Background: Cardiovascular diseases (CVDs) are a significant cause of mortality worldwide and are characterized by severe atherosclerosis (AS) in patients. However, the molecular mechanism of AS formation remains elusive. In the present study, we investigated the role of syndecan-4 (SDC4), a member of the syndecan family, in atherogenesis. Methods and Results: The expression of SDC4 decreased in mouse severe AS models. Moreover, knockout of SDC4 accelerated high-cholesterol diets (HCD)-induced AS in ApoE(-/-) mice. Mechanistically, the decrease of SDC4 increased macrophage proinflammatory capacity may be through the PKC alpha-ABCA1/ABCG1 signaling pathway. Conclusion: These findings provide evidence that SDC4 reduction links macrophages and inflammation to AS and that SDC4 in macrophages provides a therapeutic target for preventing AS formation.
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页数：13
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