Toll-like receptors and damage-associated molecular patterns in the pathogenesis of heart transplant rejection.
Cardiac transplant rejection
Coronary heart disease
DAMPs
Sterile inflammation
TLRs
Journal
Molecular and cellular biochemistry
ISSN: 1573-4919
Titre abrégé: Mol Cell Biochem
Pays: Netherlands
ID NLM: 0364456
Informations de publication
Date de publication:
Dec 2022
Dec 2022
Historique:
received:
21
02
2022
accepted:
31
05
2022
pubmed:
10
6
2022
medline:
24
11
2022
entrez:
9
6
2022
Statut:
ppublish
Résumé
Significant strides have been made in our understanding of the immune system and its role in cardiac transplant rejection. Despite the growing knowledge of immune responses, the mortality rate following cardiac transplantation remains grim. Related to procedural and pathological complications, toll-like receptor (TLR) and damage-associated molecular pattern (DAMP) signaling is the most direct and earliest interface between tissue integration and the innate immune response. This in turn can activate an adaptive immune response that further damages myocardial tissue. Furthermore, relevant literature on the status of DAMPs in the context of heart-transplantation remains limited, warranting further attention in clinical and translational research. This review aims to critically appraise the perspectives, advances, and challenges on DAMP-mediated innate immune response in the immune-mediated rejection of cardiac transplantation. Detailed analysis of the influence of TLR and DAMP signaling in mounting the immune response against the transplanted heart holds promise for improving outcomes through early detection and prevention of varied forms of organ rejection.
Identifiants
pubmed: 35678986
doi: 10.1007/s11010-022-04491-4
pii: 10.1007/s11010-022-04491-4
doi:
Substances chimiques
Toll-Like Receptors
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
2841-2850Informations de copyright
© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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