ArticleJournal of advanced research2024
In pre-clinical study fetal hypoxia caused autophagy and mitochondrial impairment in ovary granulosa cells mitigated by melatonin supplement.
Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Lipidomic Remodeling by HILPDA in Granulosa Cells Impairs Ovarian Reserve Through Disruption of Mitochondrial and Endoplasmic Reticulum Homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Mouse Mesonephros Promotes Differentiation of Oogonial Stem Cells into Follicle-like Structures via the PI3K/AKT Signaling Pathway.International journal of molecular sciences · 2026Article
- Melatonin beyond chronobiology: integrating pharmacokinetics, dose-exposure forecasting, and clinical evidence.Molecular biology reports · 2026Review
- Melatonin in ovarian function and dysfunction: Molecular mechanisms and therapeutic potential.Journal of ovarian research · 2026Review
- Establishment and identification of immortalized sheep ovarian granulosa cells.BMC veterinary research · 2026Article
- Melatonin induces autophagy in neuroblastoma by alleviating Pak2‑mediated endoplasmic reticulum stress.Molecular medicine reports · 2026Article
- Melatonin: a promising therapy to combat type 2 airway inflammation via MT1-Sirt1 pathway.Frontiers in pharmacology · 2026Article
- Maternal hypoxia exposure perturbs imprinted gene methylation in adult sperm and induces intergenerational placental impairments in male offspring.Zoological research · 2025Article
- The Regulation of ZAR1 on Apoptosis and Mitophagy in Ovarian Granular Cells and Primary Ovarian Insufficiency (POI) Mice.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Autophagy in ovary: protective roles, pathological consequences, and unresolved issues.Journal of ovarian research · 2025Review
- Melatonin refines ovarian mitochondrial dysfunction in PCOS by regulating the circadian rhythm gene Clock.Cellular and molecular life sciences : CMLS · 2025Article
- Melatonin alleviates high temperature exposure induced fetal growth restriction via the gut-placenta-fetus axis in pregnant mice.Journal of advanced research · 2025Article
- The dual nature of immunotherapy in female reproductive disorders: immune homeostasis and clinical challenges.Frontiers in immunology · 2025Review
- Lactate Promotes Hypoxic Granulosa Cells' Autophagy by Activating the HIF-1α/BNIP3/Beclin-1 Signaling Axis.Genes · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionFetal hypoxia has long-term effects on postnatal reproductive functions and the mitochondrial impairments of ovarian granulosa cells may be one of the causes. Melatonin applied to mitigate mitochondrial dysfunction and autophagy in mammalian cells has been reported. However, the potential mechanisms by which fetal hypoxia damages reproductive function in neonatal female mice and the melatonin effects on this problem remain unclear.
objectivesThis research aimed to explore the mechanism that fetal hypoxia damages reproductive function in neonatal female mice and attempt to improve the reproductive function by treating with melatonin in vivo and in vitro.
methodsWe established a fetal hypoxia model and confirmed that fetal hypoxia affects ovarian function by inducing GC excessive autophagy. Transcriptomic analysis, gene interference, cell immunofluorescence, immunohistochemistry and western blot were conducted to explore and verify the underlying mechanisms in mice GCs and KGN cells. Finally, melatonin treatment was executed on hypoxia-treated mice GCs and KGN cells and melatonin injection to fetal-hypoxia-treated mice to determine its effect.
resultsThe results of in vitro experiments found that fetal hypoxia led to mitochondrial dysfunction in ovarian GCs causing autophagic cell death. And the PI3K/Akt/FoxO pathway mediated the occurrence of this process by transcriptome analysis of ovarian GCs from normal and fetal hypoxia mice, which was further verified in mice GCs and KGN cells. Additionally, melatonin administration prevented autophagic injuries and mitochondrial impairments in hypoxia-treated mice GCs and KGN cells. Meanwhile, in vivo experiments by melatonin injection ameliorated oxidative stress of ovary in fetal-hypoxia-treated mice and improved their low fertility.
conclusionOur data found that fetal hypoxia causes ovarian GCs excessive autophagy leading to low fertility in neonatal female mice and mitigated by melatonin. These results provide a potential therapy for hypoxic stress-related reproductive disorders.
Indexed as
Identifiers
What OpenQuestion holds
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.