Activation mechanisms and multifaceted effects of mast cells in ischemia reperfusion injury.
Degranulation
Inflammatory response
Ischemia reperfusion
Mast cells
Journal
Experimental cell research
ISSN: 1090-2422
Titre abrégé: Exp Cell Res
Pays: United States
ID NLM: 0373226
Informations de publication
Date de publication:
15 03 2019
15 03 2019
Historique:
received:
26
09
2018
revised:
20
01
2019
accepted:
31
01
2019
pubmed:
5
2
2019
medline:
27
5
2020
entrez:
5
2
2019
Statut:
ppublish
Résumé
Mast cells (MCs) are tissue resident effector cells that form an important part of the immune system's first-line of defence against various pathogenic challenges. They are well known for their roles in anaphylaxis and allergy; however, increasing evidence implicates MCs in a wide range of pathologies. Ischemia/reperfusion (I/R) injury elicits an inflammatory response and triggers the program of tissue damage and restoration, as well as immune regulation. MCs are uniquely distributed around microvasculature and potentially the first responders to early or specific aspects of IR pathogenesis through the release of preformed mediators of MC granule. Versatility and extreme heterogeneity are hallmarks of MCs, resulting from different adaptions acquired during phylogenesis; such plasticity is also highlighted during MC development. Thus, it is necessary to discuss the functions of the MC population that could differ depending on the tissue in which they reside, and various effects of MCs can be induced by stimuli during I/R. In this review, we primarily discuss the contribution of MC activation in I/R injuries of hepatic, pulmonary, myocardial, cerebral, renal, and intestinal organs or systems. A further understanding of the mechanisms underlying the role of MCs in I/R injuries would aid the development of specific MC-targeted therapeutics to protect against some specific injury, such as negating the proinflammatory roles of some specific MC mediators.
Identifiants
pubmed: 30716302
pii: S0014-4827(18)31020-6
doi: 10.1016/j.yexcr.2019.01.022
pii:
doi:
Substances chimiques
Inflammation Mediators
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
227-235Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.