ArticleReproductive sciences (Thousand Oaks, Calif.)2023
Targeted Deletion of Mitofusin 1 and Mitofusin 2 Causes Female Infertility and Loss of Follicular Reserve.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Oocyte-specific acylglycerol kinase loss leads to infertility in mice via mitochondrial dysfunction.Communications biology · 2026Article
- Acetate ameliorates ovarian mitochondrial dysfunction in letrozole-induced polycystic ovarian syndrome rat model by improving mitofusin-2.The journal of physiological sciences : JPS · 2024Article
- Mitochondrial Unfolded Protein Response GeneInternational journal of molecular sciences · 2024Article
- Mechanisms of mitochondrial dysfunction in ovarian aging and potential interventions.Frontiers in endocrinology · 2024Review
- Significance of Mitochondrial Dynamics in Reproductive Physiology: Current and Emerging Horizons in Mitochondrial Therapy for Assisted Reproductive Technologies.Reproductive medicine and biologyReview
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are dynamic organelles that regulate their size, shape, and morphology through mechanisms called fusion and fission, to continually adapt themselves to their bioenergetic environment. These mechanisms play a critical role to maintain the mitochondrial function under metabolic and environmental stress. Mitofusin 1 (MFN1) and mitofusin 2 (MFN2) are transmembrane GTPases that regulate mitochondrial fusion mechanism and are required for the maintenance of cellular homeostasis. In this study, we aimed to determine the role of mitofusins in female reproductive competence and senescence using a mouse model with oocyte-specific double deletion of Mfn1 and Mfn2, eliminating the potential functional redundancy of these two proteins. Oocyte-specific targeted double deletion of Mfn1 and Mfn2 in mice resulted in female infertility associated with impaired follicular development and oocyte maturation. It also resulted in altered mitochondrial dynamics and mitochondrial dysfunction. Lack of Mfn1 and Mfn2 in oocytes resulted in accelerated follicular depletion and impaired oocyte quality which are consistent with phenotype of reproductive aging.
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Registered trials
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