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PCSK9 inhibitor Evolocumab alleviates atherosclerosis progression by suppressing endothelial cell injury via the ROS/MAPK pathway.

PCSK9 inhibitor Evolocumab alleviates atherosclerosis progression by suppressing endothelial cell injury via the ROS/MAPK pathway.

期刊: General physiology and biophysics 日期: 2026-03-01 PMID: 42281501 DOI: 10.4149/gpb_2025043 浏览: 50
作者: Ma M, Liu F, Yin X, Yue J, Duan Y, Tang J
M, M., F, L., X, Y., J, Y., Y, D., & J, T. (2026). PCSK9 inhibitor Evolocumab alleviates atherosclerosis progression by suppressing endothelial cell injury via the ROS/MAPK pathway.. General physiology and biophysics. https://doi.org/10.4149/gpb_2025043
M M, F L, X Y, J Y, Y D, J T. PCSK9 inhibitor Evolocumab alleviates atherosclerosis progression by suppressing endothelial cell injury via the ROS/MAPK pathway.. General physiology and biophysics. 2026; doi: 10.4149/gpb_2025043
M M, F L, X Y, et al. PCSK9 inhibitor Evolocumab alleviates atherosclerosis progression by suppressing endothelial cell injury via the ROS/MAPK pathway.[J]. General physiology and biophysics. 2026. DOI: 10.4149/gpb_2025043.
@article{m2026,
  author = {Ma M and Liu F and Yin X and Yue J and Duan Y and Tang J},
  title = {PCSK9 inhibitor Evolocumab alleviates atherosclerosis progression by suppressing endothelial cell injury via the ROS/MAPK pathway.},
  journal = {General physiology and biophysics},
  year = {2026},
  doi = {10.4149/gpb_2025043},
  note = {PMID: 42281501},
}
TY  - JOUR
AU  - Ma M
AU  - Liu F
AU  - Yin X
AU  - Yue J
AU  - Duan Y
AU  - Tang J
TI  - PCSK9 inhibitor Evolocumab alleviates atherosclerosis progression by suppressing endothelial cell injury via the ROS/MAPK pathway.
T2  - General physiology and biophysics
PY  - 2026
DO  - 10.4149/gpb_2025043
AN  - PMID:42281501
ER  - 

摘要

Atherosclerosis (AS) progression is closely linked to oxidized low-density lipoprotein (Ox-LDL)-induced endothelial cell injury. This study investigates the molecular mechanism by which the PCSK9 inhibitor Evolocumab (EVC) alleviates AS. We used Ox-LDL-induced HUVECs and high-fat diet (HFD)-fed ApoE-/- mice as in vitro and in vivo AS models. AS plaque formation was detected by HE and Oil Red O staining. The levels of lipid indicators and oxidative stress-related factors were measured via ELISA. The expression levels of PCSK9, apoptosis-related proteins, and signaling pathway-related proteins were determined via Western blotting. The result shows that EVC improved blood lipids and alleviated aortic injury in atherosclerotic mice, and concomitantly suppressed Ox-LDL-induced apoptosis and oxidative stress in HUVECs. In terms of the molecular mechanism, EVC attenuated the Ox-LDL-induced phosphorylation of ERK1/2, JNK and p38. Both the ROS inhibitor N-acetylcysteine and the p38 MAPK signaling pathway inhibitor SB203580 can enhance the suppressive effect of the PCSK9 inhibitor EVC on Ox-LDL induced apoptosis and oxidative stress in HUVECs, while the p38 MAPK signaling pathway activator C16-PAF shows the opposite results. In conclusion, the PCSK9 inhibitor EVC inhibits Ox-LDL-induced HUVECs apoptosis and oxidative stress by inhibiting the ROS/MAPK signaling pathway, thereby alleviating the progression of AS.

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