Role of innate immunity in cardiac inflammation after myocardial infarction.

Détails

ID Serval
serval:BIB_460D95215A0F
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Role of innate immunity in cardiac inflammation after myocardial infarction.
Périodique
Frontiers in Bioscience (Scholar Edition)
Auteur(s)
Liaudet L., Rosenblatt-Velin N.
ISSN
1945-0524 (Electronic)
ISSN-L
1945-0516
Statut éditorial
Publié
Date de publication
2013
Peer-reviewed
Oui
Volume
5
Pages
86-104
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; ReviewPublication Status: epublish
Résumé
Over the past two decades, inflammation has emerged as a key pathophysiological process during myocardial infarction. It develops consecutively to the activation of innate immune defense mechanisms, in response to the release of endogenous molecules by necrotic cells and the extracellular matrix. These danger signals are sensed by cellular receptors normally involved in antimicrobial defenses, including toll-like receptors and a subset of NOD-like receptors, which promote intracellular signaling dependent on nuclear factor kappaB and on the formation of the inflammasome. These mechanisms stimulate the expression of multiple inflammatory mediators and growth factors, sequentially inducing the recruitment of inflammatory cells, the clearance of injured tissue, angiogenesis, and the proliferation of fibroblasts, eventually resulting in scar formation and infarct healing. Dysregulation of these responses may result in continued cardiomyocyte loss, fibrosis beyond the limits of the infarcted area, reactive hypertrophy and chamber dilatation, a process termed adverse cardiac remodeling, leading to functional compromise and heart failure. This review presents the current state of knowledge on the process of immune activation within the infarcted myocardium and its consequences.
Mots-clé
Animals, Humans, Immunity, Innate, Myocardial Infarction/immunology, Myocarditis/immunology
Pubmed
Création de la notice
03/03/2014 16:32
Dernière modification de la notice
03/03/2018 16:47
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