Emerging Roles of Inflammasomes in Cardiovascular Diseases

Cardiovascular diseases are known as the leading cause of morbidity and mortality worldwide. As an innate immune signaling complex, inflammasomes can be activated by various cardiovascular risk factors and regulate the activation of caspase-1 and the production and secretion of proinflammatory cytok...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in immunology Vol. 13; p. 834289
Main Authors Liao, Yingnan, Liu, Kui, Zhu, Liyuan
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 07.04.2022
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Cardiovascular diseases are known as the leading cause of morbidity and mortality worldwide. As an innate immune signaling complex, inflammasomes can be activated by various cardiovascular risk factors and regulate the activation of caspase-1 and the production and secretion of proinflammatory cytokines such as IL-1β and IL-18. Accumulating evidence supports that inflammasomes play a pivotal role in the progression of atherosclerosis, myocardial infarction, and heart failure. The best-known inflammasomes are NLRP1, NLRP3, NLRC4, and AIM2 inflammasomes, among which NLRP3 inflammasome is the most widely studied in the immune response and disease development. This review focuses on the activation and regulation mechanism of inflammasomes, the role of inflammasomes in cardiovascular diseases, and the research progress of targeting NLRP3 inflammasome and IL-1β for related disease intervention.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
Edited by: Guo-Chang Fan, University of Cincinnati, United States
This article was submitted to Inflammation, a section of the journal Frontiers in Immunology
Reviewed by: Andrea Baragetti, University of Milan, Italy; Xuchu Que, University of California, San Diego, United States; Hui-hui Yang, Central South University, China
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2022.834289