甲状腺刺激激素通过亲环蛋白 D 乙酰化触发肝线粒体应激。
Thyroid Stimulating Hormone Triggers Hepatic Mitochondrial Stress through Cyclophilin D Acetylation.
机构信息
Shandong Institute of Endocrine & Metabolic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan 250014, China.
Department of Anesthesiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250021, China.
出版信息
Oxid Med Cell Longev. 2020 Jan 6;2020:1249630. doi: 10.1155/2020/1249630. eCollection 2020.
BACKGROUND & AIMS: Oxidative stress-related liver diseases were shown to be associated with elevated serum thyroid stimulating hormone (TSH) levels. Mitochondria are the main source of cellular reactive oxygen species. However, the relationship between TSH and hepatic mitochondrial stress/dysfunction and the underlying mechanisms are largely unknown. Here, we focused on exploring the effects and mechanism of TSH on hepatic mitochondrial stress.
METHODS
As the function of TSH is mediated through the TSH receptor (TSHR), mice and liver-specific mice and liver-specific mice and liver-specific.
RESULTS
A relatively lower degree of mitochondrial stress was observed in the livers of mice and liver-specific . Microarray and RT-PCR analyses showed that mice and liver-specific.
CONCLUSIONS
TSH stimulates hepatic CypD acetylation through the lncRNA-AK044604/SIRT1/SIRT3 signaling pathway, indicating an essential role for TSH in mitochondrial stress in the liver.
背景与目的
氧化应激相关的肝脏疾病与血清促甲状腺激素（TSH）水平升高有关。线粒体是细胞内活性氧的主要来源。然而，TSH 与肝线粒体应激/功能障碍之间的关系及其潜在机制在很大程度上尚不清楚。在这里，我们专注于探索 TSH 对肝线粒体应激的影响及其机制。
方法
由于 TSH 的功能是通过 TSH 受体（TSHR）介导的，我们构建了 TSHR 敲除（KO）小鼠和肝特异性 TSHR 敲除（LKO）小鼠和肝特异性。
结果
与野生型（WT）小鼠相比，LKO 小鼠的肝脏线粒体应激程度较低。微阵列和 RT-PCR 分析显示，LKO 小鼠和肝特异性。
结论
TSH 通过长链非编码 RNA-AK044604/SIRT1/SIRT3 信号通路刺激肝 CypD 乙酰化，表明 TSH 在肝脏线粒体应激中起重要作用。
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