REVIEW article
Front. Physiol.
Sec. Vascular Physiology
Volume 16 - 2025 | doi: 10.3389/fphys.2025.1638694
Endoplasmic Reticulum Associated Degradation mitigates Atherosclerosis by maintaining cellular homeostasis
Provisionally accepted
- 1Zhongshan People's Hospital, Zhongshan, China
- 2Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China
- 3Xiamen Medical College, Xiamen, China
- 4Sun Yat-Sen University, Guangzhou, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Atherosclerosis (AS) is a fatal cardiovascular disease that threatens human health. Although there are some treatments for AS in clinical practice, cardiovascular complications such as myocardial ischemia and hypoxia, heart failure, and stroke often occur in different AS subgroups. Therefore, it is critical and necessary to screen and identify novel protein molecules to mitigate this disease. Unstable plaques of AS is the main reason causing the fatal consequences, so it is particularly urgent to find a treatment to stabilize plaques to prevent cardiovascular and cerebrovascular diseases.During the formation of plaque, large amount of protein is produced and misfolded, this process initiates endoplasmic reticulum stress (ERS). Despite unfolded protein response (UPR) in the clearing of unfolded proteins, endoplasmic reticulum (ER) associated degradation (ERAD) maintains ER proteostasis in mammalian cells by degrading misfolded proteins. However, the role of ERAD has not been fully elucidated in AS. In this review, the role of ERS in the different cells that took part in AS was summarized, then the rescue function of ERAD in all the cell types was elucidated, especially vascular smooth muscle cells. An updated summary of the recent studies and systematic knowledge of ERAD in the mechanism of AS was presented, which may help guide future research and provide novel insights into the prevention and treatment of related diseases.
Keywords: Atherosclerosis, ERS, ERAD, Hrd1, vascular smooth muscle cell
Received: 31 May 2025; Accepted: 30 Jul 2025.
Copyright: © 2025 Niu, Wu, Cai, Yu, Lin, Cai, Chen and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Linli Wang, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.