ReviewApoptosis : an international journal on programmed cell death2025
Mechanistic study on the role of multi-pathway autophagy in ovarian aging: literature review.
Review in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Dual Roles of Autophagy in Endometrial Fibrosis and Its Implications in Age-Related Reproductive Dysfunction.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Lysine-specific demethylase 3A (KDM3A) protects against ovarian dysfunction in premature ovarian insufficiency by transcriptional activation of ATP-binding cassette sub-family A member 7 (ABCA7)-mediated mitochondrial homeostasis.Molecular biomedicine · 2026Article
- The role of mTOR signaling in regulating the quality of mammalian oocytes.Journal of assisted reproduction and genetics · 2026Review
- Fisetin Attenuates D-Gal-Induced Ovarian Aging by Modulating Mitophagy via the AMPK/mTOR Pathway.Antioxidants (Basel, Switzerland) · 2026Article
- Mechanisms of Phthalate-Induced Accelerated Ovarian Aging in Experimental Models.Current environmental health reports · 2026Review
- Bioactive natural products predominantly derived from Chinese herbal medicines for diminished ovarian reserve: mechanistic insights into ovarian protection.Frontiers in endocrinology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Ovarian aging is one of the common diseases in the female reproductive system. It is characterized by complex etiologies, involving multiple factors such as genetics, environment, metabolism, and cellular stress. In recent years, autophagy, a crucial cellular self-degradation and repair mechanism, has received substantial attention for its role in maintaining and deteriorating ovarian function. This review systematically summarizes the molecular mechanisms of autophagy and its regulation, as well as the latest research progress of macroautophagy, chaperone-mediated autophagy (CMA) and mitophagy in ovarian aging. Studies have shown that dysregulation of autophagic pathways is closely associated with decreased oocyte quality and reduced ovarian reserve function. Additionally, signaling pathways such as PI3K, AMPK, and mTOR participate in the process of ovarian aging by regulating autophagic activity. Although numerous studies have revealed the critical role of autophagy in ovarian aging, many issues remain to be resolved, such as the crosstalk mechanisms between different autophagic pathways and the precise spatiotemporal dynamics of the autophagic regulatory network. A deep understanding of the regulatory network of multi-pathway autophagy will provide new insights for developing intervention strategies to delay ovarian aging, holding significant scientific and clinical application value.
Indexed as
Identifiers
40956551What Socratic 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 Socratic graph.