Knockdown circ_0040414 inhibits inflammation, apoptosis and promotes the proliferation of cardiomyocytes via miR-186-5p/PTEN/AKT axis in chronic heart failure.
Adult
Aged
Apoptosis
/ genetics
Cell Line, Tumor
Cell Proliferation
/ genetics
Chronic Disease
Female
Heart Failure
/ genetics
Humans
Inflammation
/ genetics
Male
MicroRNAs
/ genetics
Middle Aged
Myocytes, Cardiac
/ metabolism
PTEN Phosphohydrolase
/ metabolism
Proto-Oncogene Proteins c-akt
/ metabolism
RNA, Circular
/ genetics
Signal Transduction
Circ_0040414
apoptosis
cardiomyocytes
inflammatory
proliferation
Journal
Cell biology international
ISSN: 1095-8355
Titre abrégé: Cell Biol Int
Pays: England
ID NLM: 9307129
Informations de publication
Date de publication:
Nov 2021
Nov 2021
Historique:
revised:
07
07
2021
received:
28
03
2021
accepted:
20
07
2021
pubmed:
10
8
2021
medline:
17
2
2022
entrez:
9
8
2021
Statut:
ppublish
Résumé
Previous studies have shown that circ_0040414 is highly expressed in the blood of patients with heart failure (HF), which suggests that circ_0040414 is associated with heart failure (HF). However, the functional involvement of circ_0040414 in HF and its potential mechanism remains unclear. Consistent with previous studies, our study showed that the expression of circ_0040414 in the peripheral blood of patients with chronic heart failure (CHF) was significantly higher than that of healthy control, which indicated that circ_0040414 could be used as a diagnostic biomarker in patients with CHF. In cardiomyocytes, circ_0040414 increased the level of proapoptotic proteins Bax, cleaved-caspase 3 and reduced the expression of antiapoptotic protein Bcl-2. It also promoted inflammatory factors IL-6, TNF-α, and IL-β, but inhibited cell proliferation. In terms of mechanism, circ_0040414 upregulated the expression of phosphatase and tensin homolog (PTEN) through sponging miR-186-5p to inhibit AKT signaling activity. Our study uncovered a novel role and the mechanism of circ_0040414 in controlling CHF, enriched the molecular regulatory network in CHF, and may provide a possible strategy for the treatment of CHF.
Substances chimiques
MIRN186 microRNA, human
0
MicroRNAs
0
RNA, Circular
0
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
PTEN Phosphohydrolase
EC 3.1.3.67
PTEN protein, human
EC 3.1.3.67
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2304-2315Informations de copyright
© 2021 International Federation for Cell Biology.
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