Abstract
This article focuses on ovarian cancer (OC), the most lethal gynecological malignancy, whose risk is influenced by multiple factors, including genetic background, age, reproductive history, parity, obesity status, and smoking habits. Mitochondria, as the core organelles in eukaryotic cells, play a pivotal role in the initiation and progression of OC. In recent years, growing evidence has revealed a close relationship between mitochondrial dysfunction and the accelerated proliferation, enhanced invasiveness, metastasis ability, and therapy resistance of OC. This paper provides an in-depth analysis of the complex interactions between mitochondrial dysfunction and the malignant biological characteristics of OC, as well as the underlying regulatory mechanisms of mitochondrial function. Furthermore, it elaborates on how genetic variations, regulatory factors, and the tumor microenvironment (TME) influence mitochondrial function and drive the malignant progression of OC. Additionally, this paper comprehensively summarizes therapeutic strategies targeting mitochondrial dysfunction in OC, aiming to provide novel insights and strategies for clinical research and treatment.