ArticleCell death & disease2019
Mitofusin 1 is required for female fertility and to maintain ovarian follicular reserve.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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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Who cites it
59 citing papers in PubMed, 103 citations in OpenAlex.
- Mitochondria as integrative regulators of ferroptosis in the female reproductive system.Biology of reproduction · 2026Review
- NEDDylation maintains oocyte quality by stabilizing mitochondrial transcription.Science advances · 2026Article
- Article
- Targeting a novel tamoxifen-using pathway to preserve ovarian reserve in rats with experimental chemotherapy-induced ovarian failure.BMC pharmacology & toxicology · 2026Article
- Oocyte-specific knockout of eIF2 subunits causes apoptosis of mouse oocytes within the early growing follicles via mitochondrial dysfunctions and DNA damage.Cell death & disease · 2026Article
- Parkin deficiency impairs female fertility, oocyte development, fertilization and mitochondrial function in mice.npj aging · 2026Article
- Inhibiting TRIM21 Neddylation Rejuvenates Oocyte Quality in PCOS by Regulating Ubiquitination of CPT1A.Research (Washington, D.C.) · 2026Article
- Mechanisms and treatment modalities related to premature ovarian insufficiency in mitochondria: literature review.Journal of ovarian research · 2025Review
- Mitochondria-driven inflammation: a new frontier in ovarian ageing.Journal of translational medicine · 2025Review
- Luteinizing Hormone Preserves Oocyte-Granulosa Cell Communication in Growing Follicles Exposed to Chemotherapy with Alkylating Agents at the Primordial Stage in a Mouse Model.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Regulation of Mitochondrial Metabolism byCells · 2025Article
- Mitofusin 1 Drives Preimplantation Development by Enhancing Chromatin Incorporation of Histone H3.3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mitochondrial Quality Control in Ovarian Function: From Mechanisms to Therapeutic Strategies.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Article
- The role of mitophagy in female reproductive system diseases: from molecular mechanisms to therapeutic strategies.Frontiers in endocrinology · 2025Review
- Comparison of the Mitophagy and Apoptosis Related Gene Expressions in Waste Embryo Culture Medium of Female Infertility Types.Life (Basel, Switzerland) · 2024Article
- Mechanism study of YangJing ZhongYu decoction on regulating mitochondrial dynamics of ovarian granular cells and improving diminished ovarian reserve.Journal of ovarian research · 2024Article
- Type III adenylyl cyclase is essential for follicular development in female mice and their reproductive lifespan.iScience · 2024Article
- A detailed review of pharmacology of MFN1 (mitofusion-1)-mediated mitochondrial dynamics: Implications for cellular health and diseases.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Review
- 3-Methyl-4-nitrophenol Exposure Deteriorates Oocyte Maturation by Inducing Spindle Instability and Mitochondrial Dysfunction.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondria are dynamic organelles that continually adapt their structure through fusion and fission in response to changes in their bioenergetic environment. Targeted deletion of mitochondrial fusion protein mitofusin1 (MFN1) in oocytes resulted in female infertility associated with failure to achieve oocyte maturation. Oocyte-granulosa cell communication was impaired, and cadherins and connexins were downregulated, resulting in follicle developmental arrest at the secondary follicle stage. Deletion of MFN1 in oocytes resulted in mitochondrial dysfunction and altered mitochondrial dynamics, as well as accumulation of ceramide, which contributed to increased apoptosis and a reproductive phenotype that was partially rescued by treatment with ceramide synthesis inhibitor myriocin. Absence of MFN1 and resulting apoptotic cell loss also caused depletion of ovarian follicular reserve, and a phenotype consistent with accelerated female reproductive aging.
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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.