Survival motor neuron protein protects H9c2 cardiomyocytes from hypoxia-induced cell injury by reducing apoptosis.
H9c2 cells
acute myocardial infarction
apoptosis
hypoxia
survival motor neuron protein
Journal
Clinical and experimental pharmacology & physiology
ISSN: 1440-1681
Titre abrégé: Clin Exp Pharmacol Physiol
Pays: Australia
ID NLM: 0425076
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
04
09
2019
revised:
10
06
2020
accepted:
19
06
2020
pubmed:
1
7
2020
medline:
12
11
2021
entrez:
1
7
2020
Statut:
ppublish
Résumé
Hypoxia induces cell injury in cardiomyocytes and leads to the development of cardiovascular diseases. The survival motor neuron protein (SMN) is a crucial ubiquitous protein whose functional deficiency causes motor neuron loss seen in spinal muscular atrophy. SMN has shown protective effects on the cardiovascular system and the aim of the present study was to investigate the cardioprotective effects of SMN on hypoxia-induced cell injury. Cobalt chloride (CoCl Treatment with CoCl Survival motor neuron prevents hypoxia-induced cell apoptosis through inhibition of the mitochondrial apoptotic pathway, and thereby exerts a protective effect on H9c2 cardiomyocytes.
Sections du résumé
BACKGROUND
Hypoxia induces cell injury in cardiomyocytes and leads to the development of cardiovascular diseases. The survival motor neuron protein (SMN) is a crucial ubiquitous protein whose functional deficiency causes motor neuron loss seen in spinal muscular atrophy. SMN has shown protective effects on the cardiovascular system and the aim of the present study was to investigate the cardioprotective effects of SMN on hypoxia-induced cell injury.
METHODS
Cobalt chloride (CoCl
RESULTS
Treatment with CoCl
CONCLUSION
Survival motor neuron prevents hypoxia-induced cell apoptosis through inhibition of the mitochondrial apoptotic pathway, and thereby exerts a protective effect on H9c2 cardiomyocytes.
Identifiants
pubmed: 32603518
doi: 10.1111/1440-1681.13369
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1808-1815Informations de copyright
© 2020 John Wiley & Sons Australia, Ltd.
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