Abstract
The innate immune system is well recognized as the first line defense of foreign pathogens; however, it can also recognize endogenous signals released from injured tissues and induce sterile inflammation. Toll-like receptors (TLRs) and Nod-like receptors (NLRs) have been identified as its receptors, and they have been shown to play a key role in the disease processes of sterile inflammation, including myocardial infarction (MI). In particular, NLRs are the key components of the caspase-1 activating platform known as the “inflammasome,” which produces the potent proinflammatory cytokine interleukin-1β. The current article reviews the role of the innate immune system, especially TLRs and inflammasomes, in the pathophysiology of MI.
Keywords: Cytokine, inflammasome, ischemia, nod-like receptor, reperfusion, toll-like receptor.
Graphical Abstract
Current Vascular Pharmacology
Title:Role of Innate Immune System in Inflammation and Cardiac Remodeling After Myocardial Infarction
Volume: 13 Issue: 1
Author(s): Masafumi Takahashi
Affiliation:
Keywords: Cytokine, inflammasome, ischemia, nod-like receptor, reperfusion, toll-like receptor.
Abstract: The innate immune system is well recognized as the first line defense of foreign pathogens; however, it can also recognize endogenous signals released from injured tissues and induce sterile inflammation. Toll-like receptors (TLRs) and Nod-like receptors (NLRs) have been identified as its receptors, and they have been shown to play a key role in the disease processes of sterile inflammation, including myocardial infarction (MI). In particular, NLRs are the key components of the caspase-1 activating platform known as the “inflammasome,” which produces the potent proinflammatory cytokine interleukin-1β. The current article reviews the role of the innate immune system, especially TLRs and inflammasomes, in the pathophysiology of MI.
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Cite this article as:
Takahashi Masafumi, Role of Innate Immune System in Inflammation and Cardiac Remodeling After Myocardial Infarction, Current Vascular Pharmacology 2015; 13 (1) . https://dx.doi.org/10.2174/15701611113119990007
DOI https://dx.doi.org/10.2174/15701611113119990007 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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