ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
HIGD1A Alleviates Oxidative Stress Related Ovarian Hypofunction by Enhancing Granulosa Cell Functions via NF-κB/SOD2 Signaling Pathway.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Upregulated PKM2 Protects Dopaminergic Neurons From Oxidative Damage Through Nrf2 Transactivation in an MPTP-Induced Mouse Model of Parkinson's Disease.CNS neuroscience & therapeutics · 2026Article
- Identification of novel therapeutic targets for ovarian hypofunction through hormonal pathway regulation.BMC biotechnology · 2026Article
- Recombinant humanized type III collagen improves ovarian function via ITGA2-mediated mitochondrial function restoration in granulosa cells and extracellular matrix remodeling.Regenerative biomaterials · 2026Article
- Acupuncture as an adjunctive therapy in a patient with diminished ovarian reserve and recurrent IVF failure: a case report.Frontiers in medicine · 2026Article
- HIGD1A Alleviates Oxidative Stress Related Ovarian Hypofunction by Enhancing Granulosa Cell Functions via NF-κB/SOD2 Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical UniversityArticle
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Authors and funding
12 authors.
Funding
Abstract
Diminished ovarian reserve (DOR) is a physiological or pathological condition that progresses in an age-dependent manner, which is characterized by impaired ovarian follicle quality, decreased anti-Müllerian hormone levels, elevated follicle-stimulating hormone levels, and reduced antral follicle counts. Oxidative stress (OS) is one of the culprits of DOR. By imposing OS damage on various kinds of ovarian cells including granulosa cells, OS can result in ovarian hypofunction and eventually lead to female infertility. However, the underlying mechanisms have not been fully elucidated yet. In this study, HIGD1A, a mitochondrial inner membrane component, is found to be downregulated in granulosa cells upon OS exposure. By systematically studying the role of HIGD1A in regulating granulosa cell and ovarian functions as well as its corresponding mechanisms, a novel regulatory mechanism underlying OS-related female infertility is revealed, and provided a potential molecular target for anti-OS therapies.
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Registered trials
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