ReviewChinese medical journal2025
Mechanism of mitochondrial oxidative phosphorylation disorder in male infertility.
Review in Chinese medical journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed.
- Effects of quercetin in male rats' testis after consumption of permethrin: a transmission electron microscopy (TEM) study.Scientific reports · 2026Article
- Regulation of mitochondrial function during spermatogenesis and sperm maturation.Cellular & molecular biology letters · 2026Review
- Oxidative Stress-Related Programmed Cell Death in Male Infertility: Focussing on Ferroptosis.Journal of cellular and molecular medicine · 2026Review
- FBXO39 knockdown promotes spermatogenesis impairment by inducing mitochondrial dysfunction and ferroptosis via inhibiting KDM5A ubiquitination and regulating H3K4me3 demethylation.Cell biology and toxicology · 2026Article
- Integrating multi-omics and network toxicology to identify FIS1 as a key target of environmental pollutants in male infertility.Frontiers in cell and developmental biology · 2026Article
- High-Resolution Multiplexed Sequencing of Single-Cell Full-length Transcriptome Via Combinational Barcoded Tn5 Transposon Insertion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Bridging the Gap: How environmental exposures compromise male fertility and clinical Outlook.Current research in toxicology · 2026Review
- Male infertility and the risk of developing prostate cancer: a bidirectional two-sample Mendelian randomization study.European journal of medical research · 2025Article
- An experimental study on shrimp bioactive peptides restoring testicular function in a rat model of fatty liver disease via autophagy, redox balance, and energy transporters.International journal of reproductive biomedicine · 2025Article
- In vitro confirmation of estrogenic and antiandrogenic pesticide bioactivity using schild regression analysis.Toxicology and applied pharmacology · 2025Article
- scRNA-seq deciphers molecular mechanisms of endocrine disruptor 4-nonylphenol impairing spermatogenesis in mice.Cell biology and toxicology · 2025Article
- Contribution and Regulation of HIF-1α in Testicular Injury Induced by Diabetes Mellitus.Biomolecules · 2025Review
- Exploring Single-Nucleotide Polymorphisms in Primary and Secondary Male Infertility.Medical sciences (Basel, Switzerland) · 2025Article
- Article
- Improvement on mitochondrial energy metabolism ofFrontiers in pharmacology · 2025Article
- Platelet Mitochondrial Function and Endogenous Coenzyme QInternational journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractMale 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.
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