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Updated: Jan 19, 2026
Electromechanical Assessment of Optogenetically Modulated Cardiomyocyte Activity
Published on: March 5, 2020
miR-762 modulates thyroxine-induced cardiomyocyte hypertrophy by inhibiting Beclin-1
Zheng Qiang1, Beifang Jin2, Yuntao Peng2
1Department of Anatomy, Guilin Medical University, 541004, Guilin, China. qiangzheng521@outlook.com.
Insights
Thyroxine induces cardiomyocyte hypertrophy by upregulating autophagy. MicroRNA-762 (miR-762) inhibits this process by targeting Beclin-1, revealing a novel molecular mechanism.
Area of Science:
- Cardiovascular Biology
- Molecular Endocrinology
- Cellular Physiology
Background:
- Thyroxine (T4) is a key thyroid hormone influencing cardiac function.
- Thyroxine-induced cardiomyocyte hypertrophy is a complex process with incompletely understood molecular pathways.
- Autophagy, a cellular degradation process, is implicated in cardiac remodeling, but its specific role in thyroxine-induced hypertrophy requires elucidation.
Purpose of the Study:
- To investigate the role of autophagy in thyroxine-induced cardiomyocyte hypertrophy.
- To determine if microRNA-762 (miR-762) targets Beclin-1 in the context of thyroxine-induced cardiomyocyte hypertrophy.
- To elucidate the molecular mechanisms underlying thyroxine-induced cardiac remodeling.
Main Methods:
- In vivo and in vitro studies utilizing RT-PCR, Western blot, and dual luciferase reporter assays.
- Histological analyses including HE staining, Masson staining, and transmission electron microscopy.
- Immunofluorescence and assessment of autophagic markers (LC3 II/LC3 I, Beclin-1, autophagic vacuoles).
Main Results:
- Thyroxine administration significantly increased heart rate, cardiomyocyte surface area, and collagen fiber hyperplasia in vivo.
- Upregulation of hypertrophic markers (ANP, β-MHC), autophagic activity (LC3 II/LC3 I, Beclin-1, autophagic vacuoles), and downregulation of miR-762 were observed.
- Dual luciferase reporter assay confirmed Beclin-1 as a direct target of miR-762, with miR-762 mimic attenuating and inhibitor aggravating hypertrophy and autophagy.
Conclusions:
- MicroRNA-762 plays a crucial role in modulating thyroxine-induced cardiomyocyte hypertrophy.
- miR-762 exerts its effect by directly targeting and inhibiting Beclin-1 expression.
- This study reveals a novel regulatory axis involving miR-762 and Beclin-1 in the pathogenesis of thyroxine-induced cardiac hypertrophy.
Purpose:
Whether autophagy plays a key role in thyroxine-induced cardiomyocyte hypertrophy, and whether the role of autophagy in thyroxine-induced cardiomyocyte hypertrophy is related to targeting of Beclin-1 by miR-762 remains unclear. This research focused on testing these two hypotheses. Importantly, the results of this study will help us better understand the molecular mechanisms of thyroxine-induced cardiomyocyte hypertrophy.
Methods:
In vivo and in vitro, RT-PCR, western blot, and dual luciferase reporter assay were performed to understand the molecular mechanism of thyroxine-induced cardiomyocyte hypertrophy. HE staining, Masson staining, transmission electron microscopy, and immunofluorescence were used to observe intuitively changes of hearts and cardiomyocytes.
Results:
Our results showed that in vivo, serum TT3, TT4, and heart rate were significantly upregulated in the T4 group compared with the control group. Moreover, the surface area of cardiomyocytes was significantly increased in the T4 group, and the structural disorder was accompanied by obvious hyperplasia of collagen fibers. The expression of ANP, and β-MHC was significantly upregulated in the T4 group. In addition, LC3 II/LC3 I, Beclin-1 and the count of autophagic vacuoles were significantly upregulated, but miR-762 was significantly downregulated in the T4 group compared to the control group. Subsequently, a dual luciferase reporter assay suggested that Beclin-1 was the target gene of miR-762. In vitro, the results for the T3 group were consistent with the results for the T4 group. Furthermore, cardiomyocyte hypertrophy and autophagic activity were attenuated in the T3 + miR-762 mimic group compared with the T3 group. In contrast, cardiomyocyte hypertrophy and autophagic activity were aggravated in the T3 + miR-762 inhibitor group compared with the T3 group.
Conclusions:
miR-762 modulates thyroxine-induced cardiomyocyte hypertrophy by inhibiting Beclin-1.
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