Upregulation of fibroblast growth factor 2 contributes to endometriosis through SPRYs/DUSP6/ERK signaling pathway
article
OA: closed
CC0
⤵ 6 in-corpus citations
Limited metadata. Only one source feed has indexed
this record so far — no abstract, full text, or open-access copy is
available through Endo Lab. The
publisher's page (linked below)
is the canonical location for the actual content. If you have institutional
access, use "Find at my library".
AI-generated summary
Fibroblast growth factor 2 (FGF2) upregulation promotes endometriosis by activating the SPRY/DUSP6/ERK signaling pathway.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
My notes (saved in your browser only)
Condition tags
MeSH descriptors
Citation neighborhood
Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.
References (30)
- Cellular and molecular basis for endometriosis-associated infertility via openalex
- Effect of FGF2 on the activity of SPRYs/DUSP6/ERK signaling pathway in endometrial glandular epithelial cells of endometriosis. via openalex
- Elevated levels of fibroblast growth factor-2 in serum from women with endometriosis via openalex
- Endometriosis: abnormal endometrium and dysfunctional immune response via openalex
- Endometriosis: clinical features, MR imaging findings and pathologic correlation via openalex
- Endometriosis: hormone regulation and clinical consequences of chemotaxis and apoptosis via openalex
- Endometriosis: pathogenesis and treatment via openalex
- Expression of epidermal growth factor, fibroblast growth factor‐2, and platelet‐derived growth factor‐A in the eutopic endometrium of women with endometriosis via openalex
- Overexpression of TGF‑β enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway via openalex
- PI3K/Akt And ERK1/2 signalling pathways are involved in endometrial cell migration induced by 17β-estradiol and growth factors via openalex
- Possible Pathophysiological Roles of Mitogen‐Activated Protein Kinases (MAPKs) in Endometriosis via openalex
- Research Resource: Gene Expression Profile for Ectopic Versus Eutopic Endometrium Provides New Insights into Endometriosis Oncogenic Potential via openalex
- Rethinking mechanisms, diagnosis and management of endometriosis via openalex
- Theories of endometriosis via openalex
- Transcriptional Characterizations of Differences between Eutopic and Ectopic Endometrium via openalex
- W2975180864 via openalex
- W1973840148 via openalex
- W1981903023 via openalex
- W1988814797 via openalex
- W2015698672 via openalex
- W2062837681 via openalex
- W2079530552 via openalex
- W2086920665 via openalex
- W2143390537 via openalex
- W2146479629 via openalex
- W2398601466 via openalex
- W2465367340 via openalex
- W2753335511 via openalex
- W2895219392 via openalex
- W70819804 via openalex
Cited by (6)
- GPR30-mediated non-classic estrogen pathway in mast cells participates in endometriosis pain via the production of FGF2 2023
- Expression Profiles of Genes Related to Development and Progression of Endometriosis and Their Association with Paraben and Benzophenone Exposure 2023
- The Role of Quercetin for the Treatment of Endometriosis and Endometrial Cancer: A Comprehensive Review 2023
- Localização de células senescentes nas lesões de pacientes com endometriose profunda 2022
- Identification of potential repurposed drugs for treating endometriosis-associated infertility among women 2022
- Pathogenesis of Endometriosis: New Insights into Prospective Therapies 2021
Source provenance
- europepmc
- last seen: 2026-06-11T06:19:48.454388+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-05-13T22:24:31.988741+00:00
License: CC0
· commercial use OK