线粒体功能障碍与癌症的发生、进展和转移密切相关，这在包括卵巢癌在内的多种癌症中得到证实。线粒体功能障碍的增加也与癌症进展的耐药性相关，部分与其特定的微环境有关其特点是腹水、低血糖和缺氧，导致卵巢癌细胞转向线粒体呼吸以使其生存。腹膜腹水积聚是卵巢癌的一个特有特征，也是其转移扩散的主要原因，也对有效治疗提出了挑战。卵巢癌的治疗难点之一是卵巢癌组织中线粒体DNA的突变率和频率，会影响化疗药物的疗效。不同类型的多种突变可导致代谢重编程、癌细胞增殖和耐药性。有关几种线粒体功能障碍背后机制的新具体信息，提出了将各种线粒体决定因素作为卵巢癌治疗的靶标，其中包括针对特定线粒体蛋白质和磷蛋白以及癌细胞中异常积累的活性氧 (ROS)。由于该疾病的遗传和组织学异质性，需要联合治疗方法来对抗该疾病并在卵巢癌的有效治疗方面取得进展。本章将讨论（1）潜在功能障碍和疾病的线粒体脆弱性； (2)卵巢癌线粒体功能障碍； (3) 卵巢癌的治疗难点以及针对卵巢癌线粒体代谢的新的潜在治疗策略； (4) 影响卵巢癌发展的生物行为因素。© 2024。Springer Nature Switzerland AG。

Mitochondrial dysfunctions are significantly implicated in cancer initiation, progression, and metastasis, which have been shown for several cancers including ovarian cancer.An increase in mitochondrial dysfunction is also associated with drug resistance along with cancer progression, which in part is related to its specific microenvironment that is characterized by ascites, low glucose levels, and hypoxia that causes ovarian cancer cells to switch to mitochondrial respiration to enable their survival. Peritoneal ascitic fluid accumulation is a specific feature of ovarian cancer, and it is a major cause of its metastatic spread that also presents challenges for effective treatment. Among the treatment difficulties for ovarian cancer is the mutation rate and frequency of mtDNA in ovarian cancer tissue that can affect the efficiency of chemotherapeutic drugs. The varied and multiple mutations of different types enable metabolic reprogramming, cancer cell proliferation, and drug resistance.New specific information on mechanisms underlying several of the mitochondrial dysfunctions has led to proposing various mitochondrial determinants as targets for ovarian cancer therapy, which include targeting specific mitochondrial proteins and phosphoproteins as well as reactive oxygen species (ROS) that accumulate abnormally in cancer cells. Because of the genetically and histologically heterogeneous nature of the disease, combination therapy approaches will be necessary to combat the disease and achieve progress in effective treatment of ovarian cancer. This chapter will address (1) mitochondrial vulnerabilities underlying dysfunction and disease; (2) mitochondrial dysfunction in ovarian cancer; (3) present treatment difficulties for ovarian cancer and new potential treatment strategies to target ovarian cancer mitochondrial metabolism; and (4) biobehavioral factors influencing ovarian cancer development.© 2024. Springer Nature Switzerland AG.