Neuropeptide Y mediates cardiac hypertrophy through microRNA-216b/FoxO4 signaling pathway.
Angiotensin II
/ metabolism
Animals
Arginine
/ analogs & derivatives
Cardiomegaly
/ genetics
Cells, Cultured
Disease Models, Animal
Forkhead Transcription Factors
/ genetics
Humans
Male
MicroRNAs
/ agonists
Myocardium
/ cytology
Myocytes, Cardiac
/ pathology
Neuropeptide Y
/ metabolism
Primary Cell Culture
Rats
Receptors, G-Protein-Coupled
/ antagonists & inhibitors
Receptors, Neuropeptide
/ antagonists & inhibitors
Signal Transduction
/ drug effects
Cardiac hypertrophy
FoxO4
NPY1R
Neuropeptide Y
miR-216b
Journal
International journal of medical sciences
ISSN: 1449-1907
Titre abrégé: Int J Med Sci
Pays: Australia
ID NLM: 101213954
Informations de publication
Date de publication:
2021
2021
Historique:
received:
26
07
2020
accepted:
13
10
2020
entrez:
4
1
2021
pubmed:
5
1
2021
medline:
7
9
2021
Statut:
epublish
Résumé
Cardiac hypertrophy (CH) is a major risk factor for heart failure accompanied by maladaptive cardiac remodeling. The role and potential mechanism of neuropeptide Y (NPY) in CH are still unclear. We will explore the role and the mechanism of NPY inactivation (NPY-I) in CH caused by pressure overload. Abdominal aortic constriction (AAC) was used to induce CH model in rats. NPY or angiotensin II (Ang II) was used to trigger CH model
Identifiants
pubmed: 33390770
doi: 10.7150/ijms.51133
pii: ijmsv18p0018
pmc: PMC7738963
doi:
Substances chimiques
FOXO4 protein, rat
0
Forkhead Transcription Factors
0
MIRN216 microRNA, rat
0
MicroRNAs
0
Neuropeptide Y
0
Npy1r protein, rat
0
Receptors, G-Protein-Coupled
0
Receptors, Neuropeptide
0
Angiotensin II
11128-99-7
Arginine
94ZLA3W45F
BIBO 3304
O35HK034KO
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
18-28Informations de copyright
© The author(s).
Déclaration de conflit d'intérêts
Competing Interests: The authors have declared that no competing interest exists.
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