IMR Press / RCM / Volume 23 / Issue 8 / DOI: 10.31083/j.rcm2308268
Open Access Review
NLRP3 Inflammasome as a Therapeutic Target for Atherosclerosis: A Focus on Potassium Outflow
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1 Peking University Health Science Center, 100191 Beijing, China
2 Department of Cardiology, Peking University First Hospital, 100034 Beijing, China
3 Peking University Institute of Hematology, Peking University People's Hospital, 100044 Beijing, China
4 Peking University Third Hospital, 100191 Beijing, China
*Correspondence: (Zhuo-Yu An)
These authors contributed equally.
Academic Editor: Brian Tomlinson
Rev. Cardiovasc. Med. 2022, 23(8), 268;
Submitted: 7 April 2022 | Revised: 30 May 2022 | Accepted: 23 June 2022 | Published: 22 July 2022
(This article belongs to the Special Issue Inflammation and Cardiovascular Diseases)
Copyright: © 2022 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

Atherosclerosis is a risk factor for various cardiovascular diseases, and is linked to high rates of morbidity and mortality across the globe. Although numerous complex processes are involved in the development and progression of atherosclerosis, the exact mechanisms behind its pathogenesis remain unclear. Inflammation and endothelial cell damage exert a lasting effect on atherosclerosis, causing lipid and fibrous tissue accumulation in the intima of the artery to form plaques, and subsequently promoting atherosclerosis. Nod-like receptor protein 3 (NLRP3) inflammatory corpuscle is thought to be the link between lipid metabolism and inflammation. Long Potassium outflow is a vital activator of NLRP3, with a simultaneous effect as a start-up and adjustment. The majority of existing drugs for atherosclerosis targeting the NLRP3 signaling pathway target IL-1, whereas drugs targeting the critical link of potassium efflux are relatively new. This review discusses the NLRP3 inflammatory corpuscle as a critical regulator of the immunological inflammatory pathway in atherosclerosis. Moreover, current knowledge on NLRP3 inflammatory corpuscle start and activation pathways were integrated, emphasizing potassium-involved outflow-related proteins. We highlight potential treatment approaches for NLRP3 inflammatory corpuscle pathways, specifically targeting potassium outflow channels of targeted drugs. Collectively, these insights indicate that targeting the NLRP3 inflammatory corpuscle is a vital anti-inflammatory therapy for treating atherosclerosis.

NLRP3 inflammasome
potassium efflux
therapeutic target
Fig. 1.
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