» Articles » PMID: 32760860

Innate Immune Receptors, Key Actors in Cardiovascular Diseases

Overview
Date 2020 Aug 8
PMID 32760860
Citations 46
Authors
Affiliations
Soon will be listed here.
Abstract

Cardiovascular diseases (CVDs) are the leading cause of death in the industrialized world. Most CVDs are associated with increased inflammation that arises mainly from innate immune system activation related to cardiac damage. Sustained activation of the innate immune system frequently results in maladaptive inflammatory responses that promote cardiovascular dysfunction and remodeling. Much research has focused on determining whether some mediators of the innate immune system are potential targets for CVD therapy. The innate immune system has specific receptors-termed pattern recognition receptors (PRRs)-that not only recognize pathogen-associated molecular patterns, but also sense danger-associated molecular signals. Activation of PRRs triggers the inflammatory response in different physiological systems, including the cardiovascular system. The classic PRRs, toll-like receptors (TLRs), and the more recently discovered nucleotide-binding oligomerization domain-like receptors (NLRs), have been recently proposed as key partners in the progression of several CVDs (e.g., atherosclerosis and heart failure). The present review discusses the key findings related to the involvement of TLRs and NLRs in the progression of several vascular and cardiac diseases, with a focus on whether some NLR subtypes (nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain-containing receptor 3 and nucleotide-binding oligomerization domain-containing protein 1) can be candidates for the development of new therapeutic strategies for several CVDs.

Citing Articles

Identification of regulator gene and pathway in myocardial ischemia-reperfusion injury: a bioinformatics and biological validation study.

Liu Y, Sheng X, Zhao Z, Li H, Lu J, Xie L Hereditas. 2025; 162(1):35.

PMID: 40069854 PMC: 11895329. DOI: 10.1186/s41065-025-00397-5.


Metagenomic Sequencing Combined with Metabolomics to Explore Gut Microbiota and Metabolic Changes in Mice with Acute Myocardial Infarction and the Potential Mechanism of Allicin.

Gao Y, Qin G, Liang S, Yin J, Wang B, Jiang H Drug Des Devel Ther. 2025; 19:771-791.

PMID: 39925879 PMC: 11806679. DOI: 10.2147/DDDT.S504884.


Trained innate immunity as a potential link between preeclampsia and future cardiovascular disease.

Carrasco-Wong I, Sanchez J, Gutierrez J, Chiarello D Front Endocrinol (Lausanne). 2025; 15:1500772.

PMID: 39741876 PMC: 11685753. DOI: 10.3389/fendo.2024.1500772.


Role of the NOD1/Rip2 Signaling Pathway in Macrophage Inflammatory Activation Induced by ox-LDL.

Hou L, Liu J, Yuan Y, Ding Y Cardiol Res Pract. 2024; 2024:7601261.

PMID: 39640499 PMC: 11620810. DOI: 10.1155/crp/7601261.


Cardiovascular Disease May Be Triggered by Gut Microbiota, Microbial Metabolites, Gut Wall Reactions, and Inflammation.

Dicks L Int J Mol Sci. 2024; 25(19).

PMID: 39408963 PMC: 11476619. DOI: 10.3390/ijms251910634.


References
1.
Gong T, Liu L, Jiang W, Zhou R . DAMP-sensing receptors in sterile inflammation and inflammatory diseases. Nat Rev Immunol. 2019; 20(2):95-112. DOI: 10.1038/s41577-019-0215-7. View

2.
Yu L, Feng Z . The Role of Toll-Like Receptor Signaling in the Progression of Heart Failure. Mediators Inflamm. 2018; 2018:9874109. PMC: 5822798. DOI: 10.1155/2018/9874109. View

3.
Van Tassell B, Valle Raleigh J, Abbate A . Targeting interleukin-1 in heart failure and inflammatory heart disease. Curr Heart Fail Rep. 2014; 12(1):33-41. DOI: 10.1007/s11897-014-0231-7. View

4.
Satoh M, Tabuchi T, Itoh T, Nakamura M . NLRP3 inflammasome activation in coronary artery disease: results from prospective and randomized study of treatment with atorvastatin or rosuvastatin. Clin Sci (Lond). 2013; 126(3):233-41. DOI: 10.1042/CS20130043. View

5.
Chen H, Zhang R, Wei X, Ren X, Gao X . Mechanism of TLR-4/NF-κB pathway in myocardial ischemia reperfusion injury of mouse. Asian Pac J Trop Med. 2016; 9(5):503-7. DOI: 10.1016/j.apjtm.2016.03.021. View