Next Article in Journal
Metabolite and Transcriptome Profiling Analysis Provides New Insights into the Distinctive Effects of Exogenous Melatonin on Flavonoids Biosynthesis in Rosa rugosa
Previous Article in Journal
Immune-Enhancing Effects of Gwakhyangjeonggi-san in RAW 264.7 Macrophage Cells through the MAPK/NF-κB Signaling Pathways
Previous Article in Special Issue
Xenon’s Sedative Effect Is Mediated by Interaction with the Cyclic Nucleotide-Binding Domain (CNBD) of HCN2 Channels Expressed by Thalamocortical Neurons of the Ventrobasal Nucleus in Mice
 
 
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
This is an early access version, the complete PDF, HTML, and XML versions will be available soon.
Review

Inhibitors of NLRP3 Inflammasome Formation: A Cardioprotective Role for the Gasotransmitters Carbon Monoxide, Nitric Oxide, and Hydrogen Sulphide in Acute Myocardial Infarction

Department of Pharmacology and Toxicology and HeartOtago, School of Biomedical Sciences, University of Otago, Dunedin 9054, New Zealand
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2024, 25(17), 9247; https://doi.org/10.3390/ijms25179247
Submission received: 26 July 2024 / Revised: 21 August 2024 / Accepted: 21 August 2024 / Published: 26 August 2024

Abstract

Myocardial ischaemia reperfusion injury (IRI) occurring from acute coronary artery disease or cardiac surgical interventions such as bypass surgery can result in myocardial dysfunction, presenting as, myocardial “stunning”, arrhythmias, infarction, and adverse cardiac remodelling, and may lead to both a systemic and a localised inflammatory response. This localised cardiac inflammatory response is regulated through the nucleotide-binding oligomerisation domain (NACHT), leucine-rich repeat (LRR)-containing protein family pyrin domain (PYD)-3 (NLRP3) inflammasome, a multimeric structure whose components are present within both cardiomyocytes and in cardiac fibroblasts. The NLRP3 inflammasome is activated via numerous danger signals produced by IRI and is central to the resultant innate immune response. Inhibition of this inherent inflammatory response has been shown to protect the myocardium and stop the occurrence of the systemic inflammatory response syndrome following the re-establishment of cardiac circulation. Therapies to prevent NLRP3 inflammasome formation in the clinic are currently lacking, and therefore, new pharmacotherapies are required. This review will highlight the role of the NLRP3 inflammasome within the myocardium during IRI and will examine the therapeutic value of inflammasome inhibition with particular attention to carbon monoxide, nitric oxide, and hydrogen sulphide as potential pharmacological inhibitors of NLRP3 inflammasome activation.
Keywords: NLRP3; carbon monoxide; nitric oxide; hydrogen sulphide NLRP3; carbon monoxide; nitric oxide; hydrogen sulphide

Share and Cite

MDPI and ACS Style

Payne, F.M.; Dabb, A.R.; Harrison, J.C.; Sammut, I.A. Inhibitors of NLRP3 Inflammasome Formation: A Cardioprotective Role for the Gasotransmitters Carbon Monoxide, Nitric Oxide, and Hydrogen Sulphide in Acute Myocardial Infarction. Int. J. Mol. Sci. 2024, 25, 9247. https://doi.org/10.3390/ijms25179247

AMA Style

Payne FM, Dabb AR, Harrison JC, Sammut IA. Inhibitors of NLRP3 Inflammasome Formation: A Cardioprotective Role for the Gasotransmitters Carbon Monoxide, Nitric Oxide, and Hydrogen Sulphide in Acute Myocardial Infarction. International Journal of Molecular Sciences. 2024; 25(17):9247. https://doi.org/10.3390/ijms25179247

Chicago/Turabian Style

Payne, Fergus M., Alisha R. Dabb, Joanne C. Harrison, and Ivan A. Sammut. 2024. "Inhibitors of NLRP3 Inflammasome Formation: A Cardioprotective Role for the Gasotransmitters Carbon Monoxide, Nitric Oxide, and Hydrogen Sulphide in Acute Myocardial Infarction" International Journal of Molecular Sciences 25, no. 17: 9247. https://doi.org/10.3390/ijms25179247

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop