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The mechanism of 14-3-3η in thyroxine induced mitophagy in cardiomyocytes
Yalan Cui1, Yan Zhang2, Songsong Dai2
1Department of Anatomy, College of Basic Medicine, Guilin Medical University, Guilin, Guangxi, 541004, China; Clinical Pathology Department, The Second People's Hospital of China Three Gorges University, Yichang, Hubei, 443600, China.
Abstract:
Hyperthyroidism is becoming increasingly important as an independent risk factor for cardiovascular disease, eventually resulting in cardiac hypertrophy and heart failure. The 14-3-3 protein family subtypes regulate many cellular processes in eukaryotes by interacting with a diverse array of client proteins. Considering that the 14-3-3η protein protects cardiomyocytes by affecting mitochondrial function, exploring the biological influence and molecular mechanisms by which 14-3-3η alleviates the cardiac hypertrophy of hyperthyroidism is imperative. In vivo and in vitro, RT-PCR, Western blot, and Mitochondrial tracking assay were performed to understand the molecular mechanism of thyroxine-induced cardiomyocyte hypertrophy. HE staining, transmission electron microscopy, and immunofluorescence were used to observe intuitively changes of hearts and cardiomyocytes. The in vivo and in vitro results indicated that overexpression of the 14-3-3η ameliorated thyroxine-induced cardiomyocyte hypertrophy, whereas knockdown of the 14-3-3η protein aggravated thyroxine-induced cardiomyocyte hypertrophy. Additionally, overexpression of the 14-3-3η protein reduces thyroxine-induced mitochondrial damage and mitophagy in cardiomyocytes. Overexpression of 14-3-3η protein improves excessive mitophagy in the myocardium caused by thyroxine and thus prevents cardiac hypertrophy.
Insights
14-3-3η protein protects against hyperthyroidism-induced cardiac hypertrophy by improving mitochondrial function and reducing excessive mitophagy in cardiomyocytes. This finding is crucial for understanding cardiovascular disease risk factors.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Endocrinology
Background:
- Hyperthyroidism is a significant risk factor for cardiovascular disease, leading to cardiac hypertrophy and heart failure.
- The 14-3-3 protein family regulates cellular processes, with 14-3-3η showing potential protective effects on cardiomyocytes via mitochondrial function.
Purpose of the Study:
- To investigate the protective role and molecular mechanisms of 14-3-3η in alleviating hyperthyroidism-induced cardiac hypertrophy.
- To elucidate how 14-3-3η influences mitochondrial function and mitophagy in the context of hyperthyroid cardiomyopathy.
Main Methods:
- In vivo and in vitro experiments utilizing RT-PCR, Western blot, and mitochondrial tracking assays.
- Histological analysis (HE staining, transmission electron microscopy) and immunofluorescence were employed to assess cardiac and cardiomyocyte changes.
Main Results:
- Overexpression of 14-3-3η ameliorated, while knockdown aggravated, thyroxine-induced cardiomyocyte hypertrophy.
- 14-3-3η overexpression reduced mitochondrial damage and excessive mitophagy in cardiomyocytes caused by thyroxine.
Conclusions:
- 14-3-3η protein plays a protective role against hyperthyroidism-induced cardiac hypertrophy.
- Modulating 14-3-3η may offer a therapeutic strategy for preventing or treating hyperthyroid cardiomyopathy by preserving mitochondrial integrity and regulating mitophagy.
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