Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (546 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
An oocyte-containing structure in the cortex of the ovary. The oocyte is enclosed by a layer of granulosa cells providing a nourishing microenvironment (follicular fluid). The number and size of follicles vary depending on the age and reproductive state of the female. The growing follicles are divided into five stages: primary, secondary, tertiary, Graafian, and atretic. Follicular growth and steroidogenesis depend on the presence of gonadotropins.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Follicle, Ovarian; Follicles, Ovarian; Ovarian Follicles; Graafian Follicle; Follicle, Graafian; Follicles, Graafian; Graafian Follicles; Atretic Follicle.
Where it fits in the MeSH classification
- Broader topics
- Ovary
- Narrower topics
- Follicular Fluid; Granulosa Cells; Theca Cells
- See also
- Granulosa Cells; Ovum; Theca Cells
Related concepts
Research landscape
PubMed indexes 34,359 records tagged with the MeSH heading “Ovarian Follicle” (counts retrieved 2026-10-31). 6,588 of them (19.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 11,518 records.
Reviews account for 2,556 records (7.4%) and meta-analyses for 70. Randomized controlled trials number 706 (2.1%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 11,518 |
| 2000-2009 | 7,327 |
| 2010-2019 | 8,926 |
| 2020 onward | 6,588 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,556 | 7.4% |
| Meta-analyses | 70 | 0.2% |
| Randomized controlled trials | 706 | 2.1% |
Method: PubMed query "Ovarian Follicle"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The roles of MAPK signaling pathway in ovarian folliculogenesis | 2025 | Review article Design not recorded in structured metadata | 15 | cc by PMID 40660328 · DOI · PMC12257798 |
| Increased stiffness mimicking ovarian aging induces a fibroinflammatory response in follicles and impairs oocyte quality | 2026 | Research article Design not recorded in structured metadata | 12 | cc by PMID 41575513 · DOI · PMC13695885 |
| Targeting granulosa cells with engineered DFO nanoparticles for the treatment of chemotherapy-induced premature ovarian failure | 2025 | Research article Design not recorded in structured metadata | 12 | cc by PMID 40756354 · DOI · PMC12316035 |
The roles of MAPK signaling pathway in ovarian folliculogenesis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Ovarian folliculogenesis is a complex biological process critical for female fertility, intricately regulated by various signaling pathways, among which the Mitogen-Activated Protein Kinase (MAPK) signaling pathway plays a pivotal role.
- Closing excerpt
- Clinical trial number Not applicable.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (155 words)
Ovarian folliculogenesis is a complex biological process critical for female fertility, intricately regulated by various signaling pathways, among which the Mitogen-Activated Protein Kinase (MAPK) signaling pathway plays a pivotal role. This review provides a comprehensive overview of the physiological functions of MAPK signaling in key stages of folliculogenesis, including primordial follicle formation and activation, dominant follicle selection, cumulus-oocyte complex (COC) expansion, ovulation, and luteinization. The orchestrating roles of MAPK on steroidogenesis and ovarian cell death are also delineated, highlighting its essential contributions to normal reproductive function. Furthermore, we explore the implications of dysregulated MAPK signaling in ovarian aging, primary ovarian insufficiency (POI), polycystic ovary syndrome (PCOS), and ovarian hyperstimulation syndrome (OHSS). By elucidating the multifaceted roles of MAPK signaling in ovarian biology, this review aims to enhance our understanding of folliculogenesis and its associated pathologies, paving the way for future research and therapeutic interventions targeting MAPK pathways in reproductive health. Clinical trial number Not applicable.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40660328 · DOI · PMC12257798
Increased stiffness mimicking ovarian aging induces a fibroinflammatory response in follicles and impairs oocyte quality [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Reproductive aging in females is characterized by decreased ovarian reserve and oocyte quality.
- Closing excerpt
- Our findings demonstrate that follicles are highly mechanosensitive and that stiffness alone can trigger hallmarks of ovarian aging, including reduced follicle growth, reduced oocyte quality, and a fibroinflammatory phenotype potentially integrated into the oocyte via transzonal projections.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (176 words)
Reproductive aging in females is characterized by decreased ovarian reserve and oocyte quality. With aging, both mouse and human ovaries become pro-fibrotic and stiff. However, whether follicles sense and respond to microenvironmental stiffness and affect folliculogenesis and oocyte quality independent of other aging-related factors is unknown. To address this question, we cultured mouse secondary follicles in alginate hydrogels that reproduce the stiffness of reproductively young and old mice. RNA-sequencing revealed that follicles respond rapidly to increased stiffness and exhibit enrichment in genes related to inflammation and extracellular matrix remodeling. Long-term culture in stiff hydrogels resulted in reduced follicle survival, granulosa cell viability, estradiol synthesis, and oocyte quality. To begin to determine how stiffness is transmitted within the follicle, we examined transzonal projections, which mediate granulosa cell-oocyte communication and nutrient exchange. In stiff conditions, the number of transzonal projections decreased. Our findings demonstrate that follicles are highly mechanosensitive and that stiffness alone can trigger hallmarks of ovarian aging, including reduced follicle growth, reduced oocyte quality, and a fibroinflammatory phenotype potentially integrated into the oocyte via transzonal projections.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41575513 · DOI · PMC13695885
Targeting granulosa cells with engineered DFO nanoparticles for the treatment of chemotherapy-induced premature ovarian failure [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Premature ovarian failure (POF) is a prevalent and lethal adverse event that severely affects female cancer patients receiving chemotherapy.
- Closing excerpt
- Collectively, FSH-mPDA@DFO nanoparticles hold a great potential for clinical prevention and treatment of POF patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (215 words)
Premature ovarian failure (POF) is a prevalent and lethal adverse event that severely affects female cancer patients receiving chemotherapy. It is highly correlated with the collateral damage to ovarian granulosa cells caused by ferroptosis. The excessive iron accumulation in the intracellular labile iron pool (LIP) and the aberrant generation of reactive oxygen species (ROS) is the major cause of ferroptosis. No compounds with both ferroptosis inhibition functions and ovarian-targeting specificity that do not reduce systemic chemotherapeutic efficacy have been successful in treating the POF in the clinic trials. We herein in report a multifunctional FSH-mPDA@DFO nanoparticle that can prevent chemotherapy-induced DFO by targeting LIP and ROS to restrict ferroptosis. The FSH-mPDA@DFO are constructed by encapsulating deferoxamine (DFO) within mesoporous polydopamine nanoparticles conjugated with an ovarian granulosa cell-targeting peptide (FSHβ). They downregulate transferrin receptor (TFRC) expression, reduce cellular iron ion uptake, and inhibit ferritinophagy-mediated iron mobilization, thereby ameliorating LIP overload and regulating iron metabolism. More importantly, FSH-mPDA@DFO nanoparticles can specifically accumulate in the mitochondria and suppress excessive mitophagy to preserve mitochondrial integrity and attenuate iron release and ROS generation. In vivo experiments demonstrate that FSH-mPDA@DFO nanoparticles improve oocyte quantity and quality while restoring fertility and endocrine homeostasis in chemotherapy-induced POF mice. Collectively, FSH-mPDA@DFO nanoparticles hold a great potential for clinical prevention and treatment of POF patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40756354 · DOI · PMC12316035
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The physiology and clinical utility of anti-Mullerian hormone in women [4]
- Research article Intraovarian control of early folliculogenesis [5]
- Research article Ovarian damage from chemotherapy and current approaches to its protection [6]
- Research article Oocyte environment: follicular fluid and cumulus cells are critical for oocyte health [7]
- Research article Ovarian ageing: the role of mitochondria in oocytes and follicles [8]
- Research article The road to maturation: somatic cell interaction and self-organization of the mammalian oocyte [9]
References
- Zhao H, Dinh TH, Wang Y, Yang Y. The roles of MAPK signaling pathway in ovarian folliculogenesis. . 2025. PMID 40660328 · DOI · PMC12257798
- Pietroforte S, Amargant F. Increased stiffness mimicking ovarian aging induces a fibroinflammatory response in follicles and impairs oocyte quality. . 2026. PMID 41575513 · DOI · PMC13695885
- Zhang T, Sheng Z, Zhang J, Zhang H, Zhang Y, Du Y, et al.. Targeting granulosa cells with engineered DFO nanoparticles for the treatment of chemotherapy-induced premature ovarian failure. . 2025. PMID 40756354 · DOI · PMC12316035
- Dewailly D, Andersen CY, Balen A, Broekmans F, Dilaver N, Fanchin R, et al.. The physiology and clinical utility of anti-Mullerian hormone in women. Hum Reprod Update. 2014. PMID 24430863 · DOI
- Hsueh AJ, Kawamura K, Cheng Y, Fauser BC. Intraovarian control of early folliculogenesis. Endocr Rev. 2015. PMID 25202833 · DOI · PMC4309737
- Spears N, Lopes F, Stefansdottir A, Rossi V, De Felici M, Anderson RA, et al.. Ovarian damage from chemotherapy and current approaches to its protection. Hum Reprod Update. 2019. PMID 31600388 · DOI · PMC6847836
- Dumesic DA, Meldrum DR, Katz-Jaffe MG, Krisher RL, Schoolcraft WB. Oocyte environment: follicular fluid and cumulus cells are critical for oocyte health. Fertil Steril. 2015. PMID 25497448 · DOI
- May-Panloup P, Boucret L, Chao de la Barca JM, Desquiret-Dumas V, Ferré-L'Hotellier V, Morinière C, et al.. Ovarian ageing: the role of mitochondria in oocytes and follicles. Hum Reprod Update. 2016. PMID 27562289 · DOI
- Li R, Albertini DF. The road to maturation: somatic cell interaction and self-organization of the mammalian oocyte. Nat Rev Mol Cell Biol. 2013. PMID 23429793 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.