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The mechanism of 14-3-3η in thyroxine induced mitophagy in cardiomyocytes

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单位： [1]Department of Anatomy, College of Basic Medicine, Guilin Medical University, Guilin, Guangxi, 541004, China [2]Clinical Pathology Department, The Second People’s Hospital of China Three Gorges University, Yichang, Hubei, 443600, China [3]Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Key Site of National Clinical Research Center for Respiratory Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China [4]Center of Diabetic Systems Medicine, Guangxi Key Laboratory of Excellence, Guilin Medical University, Guilin, Guangxi, 541004, China

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关键词： 14-3-3η Ywhah Mitophagy Hyperthyroidism Cardiac hypertrophy

摘要：

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.Copyright © 2024 Elsevier B.V. All rights reserved.

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出版当年[2023]版：

大类 | 3 区医学

小类 | 3 区内分泌学与代谢 3 区细胞生物学

最新[2025]版：

大类 | 2 区医学

小类 | 3 区细胞生物学 3 区内分泌学与代谢

第一作者：

第一作者单位： [1]Department of Anatomy, College of Basic Medicine, Guilin Medical University, Guilin, Guangxi, 541004, China [2]Clinical Pathology Department, The Second People’s Hospital of China Three Gorges University, Yichang, Hubei, 443600, China

通讯作者：

通讯机构： [1]Department of Anatomy, College of Basic Medicine, Guilin Medical University, Guilin, Guangxi, 541004, China [4]Center of Diabetic Systems Medicine, Guangxi Key Laboratory of Excellence, Guilin Medical University, Guilin, Guangxi, 541004, China [*1]Department of Anatomy, College of Basic Medicine, Guilin Medical University, Guilin, Guangxi, 541004, China.

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