ReviewGenesis (New York, N.Y. : 2000)2025
A Comprehensive Review of Mitochondrial Complex I During Mammalian Oocyte Maturation.
Review in Genesis (New York, N.Y. : 2000), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- [Advances in the molecular genetics of nuclear gene mutations causing pediatric mitochondrial cardiomyopathy].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Pooled it
- Testicular toll with viral intrusion: Molecular insights into the impact of chronic HIV infection on male fertility.Clinical and translational medicine · 2026Article
- Advances in bovine oocyte in vitro maturation: mechanisms and strategies.Veterinary research communications · 2026Review
- Melatonin Targets Mitochondrial Redox Homeostasis: Optimizing the Intracellular Microenvironment.International journal of molecular sciences · 2026Review
- Oxidative Stress-Telomere Axis in IVF: Molecular Mechanisms, Biomarkers, and Clinical Translation.International journal of molecular sciences · 2025Review
- Mitochondrial Collapse Responsible for Chagasic and Post-Ischemic Heart Failure Is Reversed by Cell Therapy Under Different Transcriptomic Topologies.Current issues in molecular biology · 2025Article
- Exploring the protective effects of coenzyme Q10 on female fertility.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This review provides a comprehensive overview of Complex I during mammalian oocyte maturation. Complex I (NADH:ubiquinone oxidoreductase) is a crucial member of the electron transport chain and serves two principal functions during oxidative phosphorylation: NADH oxidation and proton pumping. It is located at the inner mitochondrial membrane and consists of 14 core and 31 accessory subunits that are necessary for its function and assembly. Moreover, Complex I is the primary site of reactive oxygen species (ROS) production among the different tissues. In light of the literature, it has been demonstrated that ROS and oxidative stress are significantly important among the various factors that can affect oocyte maturation. Factors such as malnutrition, alcohol use, obesity, PCOS, aging, and smoking are some of the common causes of infertility. Each one of them causes disruption in the equilibrium of the body's redox system and related with oxidative stress. During oocyte maturation, excessive ROS levels are associated with chromosomal errors and developmental insufficiency. In addition, excess oxidative stress adversely affects embryo growth and development and may cause fetal embryopathies with damage to macromolecules in the cytoskeleton. At this particular juncture, Complex I plays a key role in determining ROS production and the success of the oocyte maturation. This review evaluates mitochondrial Complex I's function, structure, and its crucial role during oocyte maturation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.