ArticleProceedings of the National Academy of Sciences of the United States of America2006
Mitochondria-related male infertility.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.
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Who cites it
99 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Humanin ameliorates diabetes-induced testicular damage in a streptozotocin-induced mouse model.Experimental physiology · 2026Article
- Docosahexaenoic acid alleviates Ornidazole toxicity related to spermatogenic dysfunction by modulating PPARγ-dependent ER-mitochondrial uncoupling.Science China. Life sciences · 2026Article
- Cross-species urinary metabolomics identifies 2-hydroxyisovalerate as a candidate biomarker for mtDNA-based disorders.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Regulation of mitochondrial function during spermatogenesis and sperm maturation.Cellular & molecular biology letters · 2026Review
- Sperm mitochondrial sheath formation - how and why?Nature reviews. Urology · 2026Review
- Comparative analysis of muscle pathologies and metabolic signaling in mouse models of mitochondrial dysfunction.Scientific reports · 2026Article
- Impact of polystyrene microplastic exposure at low doses on male fertility: an experimental study in rats.Scientific reports · 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
- Ubiquitous Expression ofLife (Basel, Switzerland) · 2025Article
- Article
- Label-free metabolic fingerprinting of motile mammalian spermatozoa with subcellular resolution.BMC biology · 2025Article
- Effects of marijuana and tobacco on male fertility and their relationship to genetic variation of mitochondrial cytochrome C oxidase genes.Scientific reports · 2025Article
- Voltage-Dependent Anion Channels in Male Reproductive Cells: Players in Healthy Fertility?Biomolecules · 2024Review
- Molecular characterization of DNAH6 and ATPase6 (Mitochondrial DNA) genes in asthenozoospermia patients in the northern region of India.BMC urology · 2024Article
- The mitochondrial protease PARL is required for spermatogenesis.Communications biology · 2024Article
- Isatin improves oligoasthenospermia caused by busulfan by regulating GSH/GPX4 axis to inhibit ferroptosis.Frontiers in pharmacology · 2024Article
- Membrane-bound receptor for advanced glycation end products (RAGE) is a stable biomarker of low-quality sperm.Human reproduction open · 2024Article
- Exploring the dynamics of exercise intensity on male fertility and reproductive health: advancements and implications for fertility research.Frontiers in reproductive health · 2024Review
- Mother's Curse effects on lifespan and aging.Frontiers in aging · 2024Review
39 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Approximately 15% of human couples are affected by infertility, and about half of these cases of infertility can be attributed to men, through low sperm motility (asthenozoospermia) or/and numbers (oligospermia). Because mitochondrial genome (mtDNA) mutations are identified in patients with fertility problems, there is a possibility that mitochondrial respiration defects contribute to male infertility. To address this possibility, we used a transmitochondrial mouse model (mito-mice) carrying wild-type mtDNA and mutant mtDNA with a pathogenic 4,696-bp deletion (DeltamtDNA). Here we show that mitochondrial respiration defects caused by the accumulation of DeltamtDNA induced oligospermia and asthenozoospermia in the mito-mice. Most sperm from the infertile mito-mice had abnormalities in the middle piece and nucleus. Testes of the infertile mito-mice showed meiotic arrest at the zygotene stage as well as enhanced apoptosis. Thus, our in vivo study using mito-mice directly demonstrates that normal mitochondrial respiration is required for mammalian spermatogenesis, and its defects resulting from accumulated mutant mtDNAs cause male infertility.
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