Related Experiment Video
Updated: Dec 9, 2025
Analyzing Oxygen Consumption Rate in Primary Cultured Mouse Neonatal Cardiomyocytes Using an Extracellular Flux Analyzer
Published on: February 13, 2019
G6PD, bond by miR-24, regulates mitochondrial dysfunction and oxidative stress in phenylephrine-induced hypertrophic
Bing Li1, Xiaotong Wang1, Ming Yu1
1Department of Cardiology, The Third Hospital of Jilin University, Changchun 130033, China; Jilin Provincial Key Laboratory for Genetic Diagnosis of Cardiovascular Disease, Changchun 130033, China; Jilin Provincial Engineering Laboratory for Endothelial Function and Genetic Diagnosis of Cardiovascular Disease, Changchun 130033, China; Jilin Provincial Molecular Biology Research Center for Precision Medicine of Major Cardiovascular Disease, Changchun 130033, China; Jilin Provincial Cardiovascular Research Institute, Changchun 130033, China.
Insights
This study reveals that miR-24 regulates glucose-6-phosphate dehydrogenase (G6PD) to protect against mitochondrial dysfunction and oxidative stress in cardiac hypertrophy (CH) cells, offering a new therapeutic target for CH.
Area of Science:
- Cardiovascular Biology
- Mitochondrial Medicine
- Molecular Cardiology
Background:
- Pathological cardiac hypertrophy (CH) is a significant risk factor for heart failure and cardiac death.
- Mitochondrial dysfunction and oxidative stress are key features of hypertrophic cardiomyocytes.
- A potential link between glucose-6-phosphate dehydrogenase (G6PD) deficiency and CH development has been proposed.
Purpose of the Study:
- To investigate the expression of G6PD in cardiac hypertrophy.
- To elucidate the regulatory role of G6PD in mitochondrial dysfunction and oxidative stress within CH cells.
- To explore the potential therapeutic implications of targeting the miR-24/G6PD pathway in CH.
Main Methods:
- An in vitro model of CH was established using phenylephrine (PE).
- Gene expression was quantified using RT-qPCR and western blotting.
- Mitochondrial function, oxidative stress markers, cell viability, and apoptosis were assessed using ELISA, commercial kits, CCK-8, and TUNEL assays.
Main Results:
- G6PD overexpression ameliorated PE-induced mitochondrial dysfunction (decreased respiration, ATP, ATP synthase, membrane potential) and cell damage (increased LDH release, apoptosis).
- G6PD overexpression counteracted PE-induced oxidative stress (increased ROS, NO, MDA; decreased SOD, CAT) and improved cell viability.
- MiR-24 was identified as a direct regulator of G6PD expression, influencing G6PD-mediated mitochondrial dysfunction and oxidative stress in CH cells.
Conclusions:
- The miR-24/G6PD axis plays a critical role in regulating mitochondrial dysfunction and oxidative stress in cardiac hypertrophy.
- Targeting the miR-24/G6PD pathway presents a novel therapeutic strategy for cardiac hypertrophy.
- This study provides new insights into the molecular mechanisms underlying CH pathogenesis and potential treatment avenues.
Aims:
Pathological cardiac hypertrophy (CH) is one of the main risk factors for heart failure and cardiac death. Mitochondrial dysfunction and oxidative stress often occur in hypertrophic cardiomyocytes. It was recently proposed that deficiency or decreased activity of glucose-6-phosphate dehydrogenase (G6PD) may be related to the development of CH. This study aimed to investigate the expression of G6PD in CH and its regulatory role in mitochondrial dysfunction and oxidative stress of CH cells.
Main Methods:
Phenylephrine (PE) was used to create an in vitro model of CH. Using RT-qPCR and western blotting, the expression levels of target mRNAs and proteins were measured. ELISA assays and commercial kits based on spectrophotometry or colorimetry were used to measure mitochondrial function and oxidative stress. TargetScan and luciferase reporter gene assays were utilized for combination prediction and validation. CCK-8 and TUNEL kit were used to determine cell viability and apoptosis.
Key Findings:
The results showed that G6PD overexpression attenuated the decreases of mitochondrial respiration, ATP, ATP synthetase and mitochondrial membrane potential induced by PE, as well as the increases of LDH release and apoptosis. Besides, PE elevated ROS activity, NO and MDA contents, and reduced SOD, CAT levels and cell viability. These effects were hindered by G6PD overexpression. MiR-24 was found to directly bind to G6PD at the motif of CUGAGCC and regulated its expression, furtherly, influenced the G6PD-mediated mitochondrial dysfunction and oxidative stress of CH cells.
Significance:
Generally, our study demonstrated that miR-24/G6PD regulates mitochondrial dysfunction and oxidative stress in CH cells, representing a new sight for CH therapy.
More Related Videos
07:14A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
09:20Author Spotlight: Exploring Mitochondrial Function and Chemical Toxicity Using Drosophila melanogaster
Published on: November 10, 2023
