Mechanism of mitochondrial oxidative phosphorylation disorder in male infertility.
10.1097/CM9.0000000000003126
- Author:
Kai MENG
1
;
Qian LIU
2
;
Yiding QIN
2
;
Wenjie QIN
3
;
Ziming ZHU
3
;
Longlong SUN
3
;
Mingchao JIANG
3
;
Joseph ADU-AMANKWAAH
4
;
Fei GAO
1
;
Rubin TAN
4
;
Jinxiang YUAN
1
Author Information
1. Collaborative Innovation Center for Birth Defect Research and Transformation of Shandong Province, Jining Medical University, Jining, Shandong 272067, China.
2. College of Basic Medical, Jining Medical University, Jining, Shandong 272067, China.
3. College of Second Clinical Medicine, Jining Medical University, Jining, Shandong 272067, China.
4. College of Basic Medical, Xuzhou Medical University, Xuzhou, Zhejiang 221004, China.
- Publication Type:Review
- MeSH:
Male;
Humans;
Infertility, Male/metabolism*;
Oxidative Phosphorylation;
Mitochondria/metabolism*;
Spermatogenesis/physiology*;
Sertoli Cells/metabolism*;
Oxidative Stress/physiology*;
Animals;
Reactive Oxygen Species/metabolism*
- From:
Chinese Medical Journal
2025;138(4):379-388
- CountryChina
- Language:English
-
Abstract:
Male infertility has become a global concern, accounting for 20-70% of infertility. Dysfunctional spermatogenesis is the most common cause of male infertility; thus, treating abnormal spermatogenesis may improve male infertility and has attracted the attention of the medical community. Mitochondria are essential organelles that maintain cell homeostasis and normal physiological functions in various ways, such as mitochondrial oxidative phosphorylation (OXPHOS). Mitochondrial OXPHOS transmits electrons through the respiratory chain, synthesizes adenosine triphosphate (ATP), and produces reactive oxygen species (ROS). These mechanisms are vital for spermatogenesis, especially to maintain the normal function of testicular Sertoli cells and germ cells. The disruption of mitochondrial OXPHOS caused by external factors can result in inadequate cellular energy supply, oxidative stress, apoptosis, or ferroptosis, all inhibiting spermatogenesis and damaging the male reproductive system, leading to male infertility. This article summarizes the latest pathological mechanism of mitochondrial OXPHOS disorder in testicular Sertoli cells and germ cells, which disrupts spermatogenesis and results in male infertility. In addition, we also briefly outline the current treatment of spermatogenic malfunction caused by mitochondrial OXPHOS disorders. However, relevant treatments have not been fully elucidated. Therefore, targeting mitochondrial OXPHOS disorders in Sertoli cells and germ cells is a research direction worthy of attention. We believe this review will provide new and more accurate ideas for treating male infertility.
