Cardiomyocyte-derived C-type natriuretic peptide diminishes myocardial ischaemic injury by promoting revascularisation and limiting fibrotic burden.
C-type natriuretic peptide
angiogenesis
fibrosis
myocardial infarction
natriuretic peptide receptor-C
Journal
Pharmacological research
ISSN: 1096-1186
Titre abrégé: Pharmacol Res
Pays: Netherlands
ID NLM: 8907422
Informations de publication
Date de publication:
05 Oct 2024
05 Oct 2024
Historique:
received:
16
09
2024
accepted:
01
10
2024
medline:
8
10
2024
pubmed:
8
10
2024
entrez:
7
10
2024
Statut:
aheadofprint
Résumé
C-type natriuretic peptide (CNP) is a significant player in the maintenance of cardiac and vascular homeostasis regulating local blood flow, platelet and leukocyte activation, heart structure and function, angiogenesis and metabolic balance. Since such processes are perturbed in myocardial infarction (MI), we explored the role of cardiomyocyte-derived CNP, and pharmacological administration of the peptide, in offsetting the pathological consequences of MI. Wild type (WT) and cardiomyocyte-restricted CNP null (cmCNP Compared to WT littermates, cmCNP Cardiomyocytes synthesize and release CNP as an intrinsic protective mechanism in response to MI that reduces cardiac structural and functional deficits; these salutary actions are primarily NPR-C-dependent. Pharmacological targeting of CNP may represent a new therapeutic option for MI.
Sections du résumé
BACKGROUND
BACKGROUND
C-type natriuretic peptide (CNP) is a significant player in the maintenance of cardiac and vascular homeostasis regulating local blood flow, platelet and leukocyte activation, heart structure and function, angiogenesis and metabolic balance. Since such processes are perturbed in myocardial infarction (MI), we explored the role of cardiomyocyte-derived CNP, and pharmacological administration of the peptide, in offsetting the pathological consequences of MI.
METHODS
METHODS
Wild type (WT) and cardiomyocyte-restricted CNP null (cmCNP
RESULTS
RESULTS
Compared to WT littermates, cmCNP
CONCLUSIONS AND IMPLICATIONS
CONCLUSIONS
Cardiomyocytes synthesize and release CNP as an intrinsic protective mechanism in response to MI that reduces cardiac structural and functional deficits; these salutary actions are primarily NPR-C-dependent. Pharmacological targeting of CNP may represent a new therapeutic option for MI.
Identifiants
pubmed: 39374886
pii: S1043-6618(24)00392-X
doi: 10.1016/j.phrs.2024.107447
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
107447Informations de copyright
Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Adrian Hobbs reports financial support was provided by British Heart Foundation. Adrian Hobbs reports a relationship with Palatin Technologies Inc that includes: consulting or advisory. Adrian Hobbs reports a relationship with PharmaIN Corporation that includes: consulting or advisory. Adrian Hobbs reports a relationship with Novo Nordisk that includes: consulting or advisory. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. CONFLICT OF INTEREST A.J.H. is a scientific advisory board member/consultant for Palatin Technologies Inc., PharmaIN and Novo Nordisk.