Triiodothyronine induces a proinflammatory monocyte/macrophage profile and impedes cardiac regeneration.
Cardiomyocyte proliferation
Heart regeneration
Immune response
Macrophage
Triiodothyronine (T3)
Journal
Journal of molecular and cellular cardiology
ISSN: 1095-8584
Titre abrégé: J Mol Cell Cardiol
Pays: England
ID NLM: 0262322
Informations de publication
Date de publication:
10 Apr 2024
10 Apr 2024
Historique:
received:
14
09
2023
revised:
05
04
2024
accepted:
09
04
2024
medline:
13
4
2024
pubmed:
13
4
2024
entrez:
12
4
2024
Statut:
aheadofprint
Résumé
Neonatal mouse hearts can regenerate post-injury, unlike adult hearts that form fibrotic scars. The mechanism of thyroid hormone signaling in cardiac regeneration warrants further study. We found that triiodothyronine impairs cardiomyocyte proliferation and heart regeneration in neonatal mice after apical resection. Single-cell RNA-Sequencing on cardiac CD45-positive leukocytes revealed a pro-inflammatory phenotype in monocytes/macrophages after triiodothyronine treatment. Furthermore, we observed that cardiomyocyte proliferation was inhibited by medium from triiodothyronine-treated macrophages, while triiodothyronine itself had no direct effect on the cardiomyocytes in vitro. Our study unveils a novel role of triiodothyronine in mediating the inflammatory response that hinders heart regeneration.
Identifiants
pubmed: 38608929
pii: S0022-2828(24)00051-8
doi: 10.1016/j.yjmcc.2024.04.007
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright © 2023. Published by Elsevier Ltd.
Déclaration de conflit d'intérêts
Declaration of competing interest All authors declare no financial or non-financial competing interests.