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Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
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Hmgcs2 is the hub gene in diabetic cardiomyopathy and is negatively regulated by Hmgcs2, promoting high
Ying Wang1, Li-Feng Ping2, Fu-Yan Bai1
1Department of Endocrinology, The Second Affiliated Hospital of Shandong First Medical University, Tai'an, China.
Immunity, Inflammation and Disease
|March 13, 2024
Summary
Diabetic cardiomyopathy (DCM) involves heart failure. This study found microRNA (miR)-363-5p inhibits Hmgcs2, reducing high glucose-induced cardiomyocyte injury and protecting heart function.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Diabetic cardiomyopathy (DCM) is a significant cause of heart failure globally.
- Identifying regulatory targets is crucial for understanding DCM pathogenesis.
- High glucose (HG) exposure induces cardiomyocyte injury, a key factor in DCM.
Purpose of the Study:
- To screen regulatory targets of DCM.
- To analyze the role of these targets in high glucose-induced cardiomyocyte injury.
- To investigate the relationship between Hmgcs2 and miR-363-5p in DCM.
Main Methods:
- Utilized GEO database for rat DCM expression chips and differential gene screening.
- Induced rat cardiomyocytes (H9C2) with high glucose (HG).
- Measured Hmgcs2 and miR-363-5p expression; analyzed binding via dual-luciferase assay; assessed cell viability, cytotoxicity, apoptosis, inflammation, and oxidative stress using various assays.
Main Results:
- Hmgcs2 identified as a vital hub gene in DCM, upregulated in HG-induced cardiomyocytes.
- Hmgcs2 downregulation improved cell viability, reduced apoptosis, and attenuated HG-induced inflammation and oxidative stress.
- miR-363-5p confirmed as the upstream miRNA of Hmgcs2; its overexpression alleviated HG-induced cardiomyocyte injury.
Conclusions:
- Hmgcs2 plays a critical regulatory role in diabetic cardiomyopathy.
- This study is the first to report that miR-363-5p inhibits Hmgcs2 expression.
- Inhibition of Hmgcs2 by miR-363-5p alleviates high glucose-induced cardiomyocyte injury, offering a potential therapeutic target for DCM.
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