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线粒体功能障碍和氧化应激在女性生殖系统疾病中的作用:对多囊卵巢综合征和子痫前期的影响

The Role of Mitochondrial Dysfunction and Oxidative Stress in Women's Reproductive Disorders: Implications for Polycystic Ovary Syndrome and Preeclampsia.

作者信息

Deer Evangeline, LaMarca Babbette, Reckelhoff Jane F, Shawky Noha M, Edwards Kristin

机构信息

Department of Pharmacology and Toxicology, Women's Health Research Center, Mississippi Center of Excellence in Perinatal Research, University of Mississippi Medical Center, Jackson, MS 39216, USA.

出版信息

Int J Mol Sci. 2025 Jul 4;26(13):6439. doi: 10.3390/ijms26136439.

Abstract

Despite decades of research, the pathophysiology of preeclampsia (PE) and polycystic ovary syndrome (PCOS) remains poorly understood. Notably, no new FDA-approved treatments for PE have emerged in over 50 years. PCOS, a common endocrine disorder, increases a woman's risk of developing PE. Both conditions share overlapping mechanisms, including insulin resistance, chronic inflammation, endothelial dysfunction, and oxidative stress. While physiological levels of reactive oxygen species (ROS) are essential for reproduction, excess ROS contributes to cellular and mitochondrial damage. This review will assess current evidence linking oxidative stress and mitochondrial dysfunction to the development of PCOS and PE, explore their shared mechanisms, and evaluate emerging therapeutic interventions. Ultimately, a comprehensive understanding of these shared mechanisms may inform strategies for early prediction, prevention, and the treatment of PE and PCOS.

摘要

尽管经过了数十年的研究,但子痫前期(PE)和多囊卵巢综合征(PCOS)的病理生理学仍未得到充分了解。值得注意的是,50多年来没有出现新的经美国食品药品监督管理局(FDA)批准的用于治疗PE的药物。PCOS是一种常见的内分泌疾病,会增加女性患PE的风险。这两种病症具有重叠的机制,包括胰岛素抵抗、慢性炎症、内皮功能障碍和氧化应激。虽然生理水平的活性氧(ROS)对生殖至关重要,但过量的ROS会导致细胞和线粒体损伤。本综述将评估将氧化应激和线粒体功能障碍与PCOS和PE的发生联系起来的现有证据,探讨它们的共同机制,并评估新出现的治疗干预措施。最终,对这些共同机制的全面理解可能为PE和PCOS的早期预测、预防及治疗策略提供依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/528e/12249776/0f444633790f/ijms-26-06439-g001.jpg

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