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Tytuł pozycji:

HMGCS2 silencing attenuates high glucose-induced in vitro diabetic cardiomyopathy by increasing cell viability, and inhibiting apoptosis, inflammation, and oxidative stress.

Tytuł:
HMGCS2 silencing attenuates high glucose-induced in vitro diabetic cardiomyopathy by increasing cell viability, and inhibiting apoptosis, inflammation, and oxidative stress.
Autorzy:
Chen D; Department of General Geriatrics Division, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Ruan X; Department of General Geriatrics Division, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Liu Y; Department of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Guangxi Academy of Medical Sciences, Nanning, Guangxi, China.
He Y; Department of General Geriatrics Division, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Źródło:
Bioengineered [Bioengineered] 2022 May; Vol. 13 (5), pp. 11417-11429.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: 2015- : Philadelphia, PA : Taylor & Francis
Original Publication: Austin : Landes Bioscience
MeSH Terms:
Diabetes Mellitus*
Diabetic Cardiomyopathies*/genetics
Diabetic Cardiomyopathies*/metabolism
Diabetic Cardiomyopathies*/pathology
Antioxidants ; Apoptosis/genetics ; Cell Survival/genetics ; Glucose/toxicity ; Humans ; Hydroxymethylglutaryl-CoA Synthase/metabolism ; Inflammation/genetics ; Inflammation/pathology ; Oxidative Stress ; Superoxide Dismutase/metabolism
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Contributed Indexing:
Keywords: Diabetic cardiomyopathy; HMGCS2; apoptosis; bioinformatics; inflammation; oxidative stress
Substance Nomenclature:
0 (Antioxidants)
0 (HMGCS2 protein, human)
EC 1.15.1.1 (Superoxide Dismutase)
EC 2.3.3.10 (Hydroxymethylglutaryl-CoA Synthase)
IY9XDZ35W2 (Glucose)
Entry Date(s):
Date Created: 20220504 Date Completed: 20220505 Latest Revision: 20220716
Update Code:
20240104
PubMed Central ID:
PMC9275940
DOI:
10.1080/21655979.2022.2063222
PMID:
35506308
Czasopismo naukowe
Diabetic cardiomyopathy (DCM) is a diabetic mellitus-related complications and progression of DCM may eventually lead to heart failure, while mechanisms related to DCM pathophysiology remain unclear. The study was undertaken to identify possible hub genes associated with DCM progression through bioinformatics analysis and to validate the role of 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) in DCM progression using a cellular model of high glucose (HG)-induced DCM. The common differentially expressed genes (DEGs) between GSE173884 and GSE161827 were used for PPI network analysis. Our results identified 17 common DEGs between GSE173384 and GSE161827. Further analysis of the protein-protein interaction network identified nine hub genes and HMGCS2. The in vitro functional assays showed that HG induced up-regulation of HMGCS2, suppressed cardiomyocyte viability, enhanced apoptosis, inflammation, and oxidative stress of cardiomyocytes. Gain-of-function assays showed that HMGCS2 overexpression reduced cell viability, increased apoptosis, caspase-3/-9 activity, up-regulated interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) expression, decreased superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase expression, increased malondialdehyde (MDA) content, and reactive oxygen species (ROS) level but inhibited total antioxidant activity, SOD activity, CAT activity, and glutathione content in cardiomyocytes. Rescue experiments demonstrated HMGCS2 silence attenuated HG-induced decrease in cardiomyocyte viability and increase in cardiomyocyte apoptosis, inflammation, and oxidative stress. All in all, our study identified HMGCS2 as a hub gene in DCM pathophysiology and further functional studies indicated that HMGCS2 may aggravate DCM progression by reducing cardiomyocyte viability, increasing cardiomyocyte apoptosis, and promoting inflammation and oxidative stress in cardiomyocytes.

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