IMR Press / RCM / Volume 23 / Issue 3 / DOI: 10.31083/j.rcm2303097
Open Access Review
Interleukin Receptor Associated Kinase 1 Signaling and Its Association with Cardiovascular Diseases
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1 Department of Biomedical Sciences and Pathobiology, College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061, USA
*Correspondence: (Jia-Qiang He)
Academic Editors: Giuseppe Biondi-Zoccai, Mariangela Peruzzi and Antonio Abbate
Rev. Cardiovasc. Med. 2022, 23(3), 97;
Submitted: 22 November 2021 | Revised: 17 January 2022 | Accepted: 29 January 2022 | Published: 12 March 2022
Copyright: © 2022 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

Toll-like receptors (TLRs) and interleukin-1 receptor (IL-1R) directly interact with intracellular interleukin receptor associated kinase (IRAK) family members to initialize innate immune and inflammatory responses following activation by pathogen-associated or host-derived elements. Although four IRAK family members [IRAK1, 2, 3 (i.e., IRAK-M), and 4] are involved in TLR and IL-1R signaling pathways, IL-1R > IRAK1 signaling appears to be the most studied pathway, with sufficient evidence to support its central role linking the innate immune response to the pathogenesis of various diseases, including cancers, metabolic disorders, and non-infectious immune disorders. However, IRAK1’s involvement in cardiovascular diseases was only recently revealed and the detailed mechanism underling the pathogenesis of cardiovascular diseases, such as atherosclerosis, myocardial infarction, and heart failure (all non-infectious disorders), remains largely unknown with very limited publications to date. This review aims to summarize the overall roles of the IRAK family, especially IRAK1, in mediating the development of cardiovascular diseases.

interleukin-1 receptor associated kinase 1
innate immune response
signaling pathways
toll-like receptor
interleukin-1 receptor
endothelial cells
vascular smooth muscle cells
myocardial infarction
heart failure
Fig. 1.
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