C5a-C5aR1 induces endoplasmic reticulum stress to accelerate vascular calcification via PERK-eIF2α-ATF4-CREB3L1 pathway.

Aiting LiuZhenwei ChenXiaoxue LiChen XieYanlian ChenXiaoyan SuYing ChenMengbi ZhangJie ChenTiecheng YangJiangang ShenHui Huang

Published in: Cardiovascular research (2023)

High level of C5a was associated with increased risk of VC, and it accelerated VC by activating the receptor C5aR1. PERK-eIF2α-ATF4-CREB3L1 pathway of endoplasmic reticulum stress was activated by C5a-C5aR1, hence promoting VSMCs osteogenic transdifferentiation. Targeting C5 or C5aR1 may be an appealing therapeutic target for VC.

Keyphrases

endoplasmic reticulum stress
induced apoptosis
mesenchymal stem cells
chronic kidney disease
signaling pathway
cancer therapy
drug delivery
oxidative stress
transcription factor
angiotensin ii
endoplasmic reticulum