Alteration of immune response and synovium microvasculature in Rheumatoid arthritis (RA) progression has been suggested to be associated with mitochondrial functioning. Mitochondria, with maternally inherited DNA, exhibit differential response to the female hormone estrogen. Various epidemiological evidence has also shown the prominence of RA in the female population, depicting the role of estrogen in modulating the pathogenesis of RA. As estrogen regulates the expression of differential proteins and associated signaling pathways of RA, its influence on mitochondrial functioning seems evident. Thus, in this review, the studies related to mitochondria and their relation with estrogen and Rheumatoid arthritis were retrieved. We analyzed the different mitochondrial activities that are altered in RA and the possibility of their estrogenic control. The study expands to analysis, revealing the differential mitochondrial proteins expressed in RA and examining these proteins as potential estrogenic targets. It was found that ALDH2, CASP3, and SOD2 are the major mitochondrial proteins involved in RA progression and are also potent estradiol targets. The analysis establishes the role of mitochondrial proteins in RA progression, which were found to be direct or indirect targets of estrogen, depicting their potential for regulating mitochondrial functions in RA.

中文翻译：

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雌激素调节类风湿性关节炎的线粒体功能：基于性别对线粒体和疾病影响的循证见解

类风湿性关节炎（RA）进展中免疫反应和滑膜微血管的改变被认为与线粒体功能有关。线粒体具有母系遗传的 DNA，对雌性激素表现出不同的反应。各种流行病学证据也显示 RA 在女性人群中的突出地位，描述了雌激素在调节 RA 发病机制中的作用。由于雌激素调节 RA 差异蛋白的表达和相关信号通路，因此它对线粒体功能的影响似乎很明显。因此，本综述检索了有关线粒体及其与雌激素和类风湿性关节炎关系的研究。我们分析了 RA 中改变的不同线粒体活性及其雌激素控制的可能性。该研究扩展到分析，揭示了 RA 中表达的差异线粒体蛋白，并检查这些蛋白作为潜在的雌激素靶点。研究发现 ALDH2、CASP3 和 SOD2 是参与 RA 进展的主要线粒体蛋白，也是有效的雌二醇靶点。该分析确定了线粒体蛋白在 RA 进展中的作用，这些蛋白被发现是雌激素的直接或间接靶标，描述了它们在 RA 中调节线粒体功能的潜力。