A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages
J Hu, Y Zhang, L Hu, H Chen, H Wu, J Chen… - Journal of Translational …, 2022 - Springer
J Hu, Y Zhang, L Hu, H Chen, H Wu, J Chen, J Xie, B Xu, Z Wei
Journal of Translational Medicine, 2022•SpringerAbstract 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 …
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 …
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 PKCα-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.
Springer
