Home General Physiology and Biophysics 2022 General Physiology and Biophysics Vol.41, No.6, p. 535–547, 2022

Journal info


Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

Aims and Scope
Editorial Info
Abstracting and Indexing
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.
Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

General Physiology and Biophysics Vol.41, No.6, p. 535–547, 2022

Title: Homocysteine promotes migration of adventitial fibroblasts via angiotensin II type 1 receptor activation to aggravate atherosclerosis
Author: Zhibo Zhu, Sujuan Li, Yuchen Jia, Jianqiang Guo
Abstract: This study clarified the effect of homocysteine on adventitial fibroblasts (AFs) and its relationship with angiotensin II type 1 receptor (AT1R). Hyperhomocysteinemia aggravated the plaque area and increased the expression of IL-6, MCP-1, and macrophage infiltration in the plaque and adventitia of the aorta, whereas telmisartan improved this effect. Hyperhomocysteinemia induced the occurrence of the AFs marker protein ER-TR7 in the plaque and entire layer of the aorta, whereas telmisartan improved these effects, indicating that homocysteine induced AFs migration and that AT1R mediated this process. The migration experiments of AFs also reached the same conclusion. Homocysteine increased the phosphorylation levels of PKC and ERK1/2 in the AFs and HEK293A cells transfected with the AT1R plasmid, whereas telmisartan inhibited this effect, indicating that homocysteine activated AT1R intracellular signaling pathway. Homocysteine also increased the AFs At1R expression. Conclusion, homocysteine promoted adventitial inflammation, induced AFs migration, and aggravated atherosclerosis by activating AT1R.
Keywords: Homocysteine — Angiotensin II type 1 receptor — Adventitial fibroblasts — Migration — Atherosclerosis
Published online: 23-Nov-2022
Year: 2022, Volume: 41, Issue: 6 Page From: 535, Page To: 547
doi:10.4149/gpb_2022039


download file


© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.