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Long Noncoding RNA H19 Overexpression Inhibits High Glucose-Induced Oxidative Stress of Cardiomyocytes by Targeting

Xuelin Liu1,2, Qian Zhang1,2, Yuemei Zhang2

  • 1Department of Cardiology, Gansu Provincial Central Hospital, Lanzhou, 730070, Gansu, China.

Biochemical Genetics
|October 2, 2025
PubMed

Insights

Long non-coding RNA H19 protects against diabetic cardiomyopathy by regulating miR-138-5p and mitochondrial calcium uniporter (MCU). This pathway reduces oxidative stress in heart cells, offering potential therapeutic targets for diabetic heart disease.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Biochemistry

Background:

  • Diabetic cardiomyopathy (DCM) involves mitochondrial oxidative stress.
  • Long non-coding RNAs (lncRNAs) play roles in cellular regulation.
  • The H19 lncRNA and miR-138-5p microRNA are implicated in various cellular processes.

Purpose of the Study:

  • To investigate the regulatory role of lncRNA H19 on miR-138-5p.
  • To determine the impact of the H19/miR-138-5p axis on mitochondrial oxidative stress in DCM.
  • To elucidate the molecular mechanisms underlying DCM pathogenesis.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) for gene expression analysis.
  • In vitro diabetic cardiomyopathy model using high glucose-exposed H9c2 cardiomyocytes.
  • Dual-luciferase reporter assays to confirm targeting relationships.
  • Western blotting for protein expression analysis.
  • Measurement of reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) to assess oxidative stress.

Main Results:

  • In the DCM model, H19 and mitochondrial calcium uniporter (MCU) were downregulated, while miR-138-5p was upregulated.
  • H19 overexpression reduced oxidative stress markers (ROS, MDA) and increased antioxidant activity (SOD) in high glucose-treated cells.
  • miR-138-5p was validated to target both H19 and MCU, suppressing MCU protein expression.
  • Rescue experiments confirmed that miR-138-5p overexpression or MCU silencing reversed the protective effects of H19.

Conclusions:

  • lncRNA H19 attenuates mitochondrial oxidative stress in diabetic cardiomyopathy by modulating the miR-138-5p/MCU axis.
  • The H19/miR-138-5p/MCU pathway is a key mechanism in DCM pathogenesis.
  • H19 shows potential as a diagnostic biomarker and therapeutic target for diabetic cardiomyopathy.
Keywords:
Diabetic CardiomyopathyLong Noncoding RNA H19MicroRNA-138-5pMitochondrial Calcium UniporterOxidative Stress

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