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

Jiaxin Hu, Ying Zhang, Liaoping Hu, Haiting Chen, Han Wu, Jianzhou Chen, Jun Xie, Biao Xu, Zhonghai Wei

Journal of translational medicine 2022 Jul 16

filter terms:

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. 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 PKCα-ABCA1/ABCG1 signaling pathway. 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. © 2022. The Author(s).

Citation

Jiaxin Hu, Ying Zhang, Liaoping Hu, Haiting Chen, Han Wu, Jianzhou Chen, Jun Xie, Biao Xu, Zhonghai Wei. A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages. Journal of translational medicine. 2022 Jul 16;20(1):319