ER Stress Activates the NLRP3 Inflammasome: A Novel Mechanism of Atherosclerosis
Joint Authors
Zhang, Junping
Chen, Xinnong
Guo, Xiaochen
Ge, Qihui
Zhao, Yixuan
Mu, Huaiyu
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-18, 18 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-10-07
Country of Publication
Egypt
No. of Pages
18
Main Subjects
Abstract EN
The endoplasmic reticulum (ER) is an important organelle that regulates several fundamental cellular processes, and ER dysfunction has implications for many intracellular events.
The nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome is an intracellularly produced macromolecular complex that can trigger pyroptosis and inflammation, and its activation is induced by a variety of signals.
ER stress has been found to affect NLRP3 inflammasome activation through multiple effects including the unfolded protein response (UPR), calcium or lipid metabolism, and reactive oxygen species (ROS) generation.
Intriguingly, the role of ER stress in inflammasome activation has not attracted a great deal of attention.
In addition, increasing evidence highlights that both ER stress and NLRP3 inflammasome activation contribute to atherosclerosis (AS).
AS is a common cardiovascular disease with complex pathogenesis, and the precise mechanisms behind its pathogenesis remain to be determined.
Both ER stress and the NLRP3 inflammasome have emerged as critical individual contributors of AS, and owing to the multiple associations between these two events, we speculate that they contribute to the mechanisms of pathogenesis in AS.
In this review, we aim to summarize the molecular mechanisms of ER stress, NLRP3 inflammasome activation, and the cross talk between these two pathways in AS in the hopes of providing new pharmacological targets for AS treatment.
American Psychological Association (APA)
Chen, Xinnong& Guo, Xiaochen& Ge, Qihui& Zhao, Yixuan& Mu, Huaiyu& Zhang, Junping. 2019. ER Stress Activates the NLRP3 Inflammasome: A Novel Mechanism of Atherosclerosis. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-18.
https://search.emarefa.net/detail/BIM-1203232
Modern Language Association (MLA)
Chen, Xinnong…[et al.]. ER Stress Activates the NLRP3 Inflammasome: A Novel Mechanism of Atherosclerosis. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-18.
https://search.emarefa.net/detail/BIM-1203232
American Medical Association (AMA)
Chen, Xinnong& Guo, Xiaochen& Ge, Qihui& Zhao, Yixuan& Mu, Huaiyu& Zhang, Junping. ER Stress Activates the NLRP3 Inflammasome: A Novel Mechanism of Atherosclerosis. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-18.
https://search.emarefa.net/detail/BIM-1203232
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1203232