ArticleCommunications biology2024
Maintaining mitochondrial DNA copy number mitigates ROS-induced oocyte decline and female reproductive aging.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Lower mitochondrial DNA copy number in ATTRV50M Swedish carriers.Orphanet journal of rare diseases · 2026Article
- Inheritance and selection of the mitochondrial genome.Nature reviews. Genetics · 2026Review
- Mitochondrial DNA leakage in oocytes activates cGAS-STING signaling to drive ovarian aging.Nature aging · 2026Article
- Crosstalk collapse: mitochondria-centric organelle network disruption in ovarian aging.Cell communication and signaling : CCS · 2026Review
- Mitochondrial dynamics imbalance in hepatocellular carcinoma: from molecular mechanisms to new strategies for targeted therapy.Translational cancer research · 2026Review
- Ethnopharmacological evaluation and metabolic mechanism of Sanjie Xiaoliu Granule in breast cancer with depression.Biological procedures online · 2026Article
- Comparative mitochondrial genome architecture and nuclear mitochondrial DNA (NUMT) landscapes in stink bugs of the family Pentatomidae.Functional & integrative genomics · 2026Article
- Moxibustion delays ovarian aging by regulating mitochondrial biogenesis and improving oocyte quality.Chinese medicine · 2026Article
- Oocyte aging in focus: Environmental and endogenous stressors driving reproductive potential decline.GeroScience · 2026Review
- Targeting MFF succinylation: a novel therapeutic strategy for premature ovarian insufficiency by restoring mitochondrial dynamics in granulosa cells.Journal of ovarian research · 2026Review
- Mitochondrion-targeted therapies for diabetic wound healing: from mechanism to therapeutic opportunity.Burns & trauma · 2026Review
- Moderate NEFA reprogram early follicular development and oocyte competence: evidence for a targetable redox mechanism.Frontiers in nutrition · 2026Article
- Deoxyguanosine kinase deficiency couples purine metabolism to innate immune activation and lipid accumulation in hepatocytes.Frontiers in immunology · 2026Article
- Research Hotspots and Emerging Frontiers in Ovarian Aging: A Bibliometric Analysis (2006-2025).Endocrine, metabolic & immune disorders drug targets · 2026Review
- The hierarchical stratum response system of organism to microgravity during spaceflight.Military Medical Research · 2026Review
- Oxidoreductase delivery by cell therapies in cyclophosphamide-induced premature ovarian insufficiency: a mechanistic insight into ovarian rejuvenation.Journal of ovarian research · 2025Article
- Mitochondria-driven inflammation: a new frontier in ovarian ageing.Journal of translational medicine · 2025Review
- Abundance of Maternal Mitochondrial Genome Is Dispensable up to the Mitochondrial Genome Activation in Post-Implantation Embryos.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Mitochondrial-Targeted Protective Potential of Elamipretide for the In Vitro Production of Porcine Embryos.Animals : an open access journal from MDPI · 2025Article
- Mitochondrial dysfunction in oocytes: implications for fertility and ageing.Journal of ovarian research · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oocytes play a crucial role in transmitting maternal mitochondrial DNA (mtDNA), essential for the continuation of species. However, the effects of mitochondrial reactive oxygen species (ROS) on mammalian oocyte maturation and mtDNA maintenance remain unclear. We investigated this by conditionally knocking out the Sod2 gene in primordial follicles, elevating mitochondrial matrix ROS levels from early oocyte stages. Our data indicates that reproductive aging in Sod2 conditional knockout females begins at 6 months, with oxidative stress impairing oocyte quality, particularly affecting OXPHOS complex II and mtDNA-encoded mRNA levels. Despite unchanged mtDNA mutation load, mtDNA copy numbers exhibited significant variations. Strikingly, reducing mtDNA copy numbers by reducing mtSSB protein, crucial for mtDNA replication, accelerated reproductive aging onset to three months, underscoring the critical role of mtDNA copy number maintenance under oxidative stress conditions. This research provides new insights into the relationship among mitochondrial ROS, mtDNA, and reproductive aging, offering potential strategies for delaying aging-related fertility decline.
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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.