Regulation of mitochondrial morphology and metabolism by Jak-STAT pathway

K. Rhee
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引用次数: 0

Abstract

regulation of mitochondria morphology and function may be crucial for finding treatments for infertility, neu-rodegenerative diseases, diabetes, obesity, and cancer. This review focuses on both the canonical and noncanonical role of the Jak-STAT pathway in mitochondrial morphology and metabolism. ABSTRACT Jak-STAT pathway is required for embryogenesis, female gametogenesis, cytokine-mediated neuroprotection, diabetes, obesity, cancer, stem cell, and various tissues. The noncanonical role of Jak-STAT in mitochondria function was supported by the detection of STAT protein in mitochondria, however, several studies show that STAT protein is detected in the endoplasmic reticulum (ER), and not in mitochondria. STAT protein may alter mitochondria function without entering mitochondria, this involves regulation of fission and fusion proteins to change mitochondria morphology. However, how changes in mitochondria morphology lead to changes in mitochondria metabolism needs further investigation.
Jak-STAT通路对线粒体形态和代谢的调控
线粒体形态和功能的调节可能是寻找治疗不孕症、神经退行性疾病、糖尿病、肥胖和癌症的关键。本文综述了Jak-STAT通路在线粒体形态和代谢中的典型和非典型作用。胚胎发生、雌性配子发生、细胞因子介导的神经保护、糖尿病、肥胖、癌症、干细胞和各种组织都需要Jak-STAT通路。线粒体中STAT蛋白的检测支持了Jak-STAT在线粒体功能中的非规范作用,然而,一些研究表明STAT蛋白在内质网(ER)中检测到,而不是在线粒体中检测到。STAT蛋白可以在不进入线粒体的情况下改变线粒体功能,这涉及到调节裂变和融合蛋白来改变线粒体形态。然而,线粒体形态的变化如何导致线粒体代谢的变化还需要进一步研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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