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Updated: Nov 28, 2025
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Circ_0010729 knockdown protects cardiomyocytes against hypoxic dysfunction via miR-370-3p/TRAF6 axis
Jingjing Zhang1, Chuanyu Gao2, Jing Zhang1
1Coronary Care Unit, Department of Cardiology, People's Hospital of Zhengzhou University, Zhengzhou City, Henan Procince, China.
Insights
Circular RNA circ_0010729 exacerbates hypoxia-induced cardiomyocyte injury in myocardial infarction. Knockdown of circ_0010729 protects against this injury by regulating the miR-370-3p/TRAF6 axis.
Area of Science:
- Cardiovascular Diseases
- Molecular Biology
- Cellular Biology
Background:
- Hypoxia-induced cell injury is a critical factor in cardiovascular diseases, particularly myocardial infarction.
- The specific regulatory mechanisms of circular RNAs, like circ_0010729, in hypoxia-induced cardiomyocyte dysfunction remain largely uncharacterized.
- Understanding these mechanisms is crucial for developing novel therapeutic strategies for myocardial infarction.
Purpose of the Study:
- To investigate the role of circ_0010729 in hypoxia-induced cardiomyocyte injury.
- To elucidate the underlying regulatory mechanism involving miR-370-3p and TRAF6.
- To assess the therapeutic potential of targeting circ_0010729 in myocardial infarction.
Main Methods:
- Cell viability, cycle, apoptosis, and migration assays were performed.
- Inflammatory factors (TNF-α, IL-6) and glucose metabolism were analyzed.
- Quantitative real-time PCR, western blot, dual-luciferase reporter, and RNA immunoprecipitation assays were employed to detect and verify molecular interactions.
Main Results:
- Hypoxia impaired cardiomyocyte function, increasing apoptosis and inflammation while inhibiting glucose metabolism.
- Circ_0010729 expression was upregulated under hypoxia and its knockdown conferred protection against hypoxic injury.
- Circ_0010729 directly interacted with miR-370-3p, and indirectly regulated TRAF6 via miR-370-3p, with miR-370-3p targeting TRAF6.
Conclusions:
- Circ_0010729 knockdown mitigates hypoxia-induced cardiomyocyte dysfunction and injury.
- The protective effect is mediated through the circ_0010729/miR-370-3p/TRAF6 axis.
- Circ_0010729 represents a potential therapeutic target for myocardial infarction treatment.
Abstract:
Few studies have addressed the mechanism by which circ_0010729 regulates hypoxia-induced cell injury in cardiovascular diseases. However, its role and its regulatory mechanism in myocardial infarction remain to be explored. Cell viability, cycle, apoptosis, and migration were analyzed using cell counting kit-8 assay, flow cytometry, caspase-3 activity assay kit and transwell assay, respectively. Tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) concentrations were examined by enzyme-linked immunosorbent assay. Glucose metabolism was calculated by detecting ATP production, glucose uptake and lactate production. Levels of circ_0010729, miR-370-3p and TNF Receptor Associated Factor 6 (TRAF6) were detected using quantitative real-time polymerase chain reaction or western blot. The direct interaction between circ_0010729 and TRAF6 or miR-370-3p was verified using dual-luciferase reporter assay and RNA immunoprecipitation assay. Under hypoxia condition, cardiomyocytes suffered from cell viability suppression, cell cycle arrest, cell apoptosis promotion, migration reduction, increase of inflammatory factor IL-6 and TNF-α, as well as glycolysis inhibition. Circ_0010729 expression was up-regulated in the cardiomyocytes at different hypoxia-exposed time points. Circ_0010729 knockdown protected cardiomyocytes against hypoxic dysfunction, while circ_0010729 overexpression showed inverse effects. MiR-370-3p was confirmed to directly bind to circ_0010729 or TRAF6. MiR-370-3p inhibition attenuated the protective effects of circ_0010729 knockdown on hypoxia-modulated cardiomyocyte dysfunction. MiR-370-3p restoration protected cardiomyocytes against hypoxic injury via targeting TRAF6. Besides, circ_0010729 indirectly regulated TRAF6 expression via miR-370-3p. This study demonstrated that circ_0010729 knockdown attenuated hypoxia-induced cardiomyocyte dysfunction via miR-370-3p/TRAF6 axis, indicating a potential therapeutic target for myocardial infarction.
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