ArticleEndocrinology2014
Krüppel-like factor 9 deficiency in uterine endometrial cells promotes ectopic lesion establishment associated with activated notch and hedgehog signaling in a mouse model of endometriosis.
Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 80 citations in OpenAlex.
- Unveiling myometrial SP/Krüppel-like factors as drivers of parturition: insights from transcriptional and endocrine regulatory networks.Endocrine connections · 2025Review
- PDLIM3 knockdown promotes ferroptosis in endometriosis progression via inducing Gli1 degradation and blocking Hedgehog signaling pathway.Journal of assisted reproduction and genetics · 2024Article
- Review
- Cross talk of tumor protein D52 (TPD52) with KLF9, PKCε, and MicroRNA 223 in ovarian cancer.Journal of ovarian research · 2023Article
- Molecular Mechanisms of Endometriosis Revealed Using Omics Data.Biomedicines · 2023Review
- A Pilot Study on the Co-existence of Diabetes and Endometriosis in Reproductive-Age Women: Potential for Endometriosis Progression.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- Krüppel-like factor 9 (KLF9) links hormone dysregulation and circadian disruption to breast cancer pathogenesis.Cancer cell international · 2023Article
- Article
- Effects of an inhibitor of the SHH signaling pathway on endometrial cells of patients with endometriosis.BMC molecular and cell biology · 2022Article
- Predicting 3D Structure, Cross Talks, and Prognostic Significance ofFrontiers in oncology · 2021Article
- Lesion Genotype Modifies High-Fat Diet Effects on Endometriosis Development in Mice.Frontiers in physiology · 2021Article
- The effects of hedgehog ligand neutralising antibody 5E1 in a mouse model of endometriosis.BMC research notes · 2020Article
- Krüppel-like factor 17 upregulates uterine corin expression and promotes spiral artery remodeling in pregnancy.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Uncovering Potential Roles of Differentially Expressed Genes, Upstream Regulators, and Canonical Pathways in Endometriosis Using an In Silico Genomics Approach.Diagnostics (Basel, Switzerland) · 2020Article
- Interleukin-6 (IL-6) Activates the NOTCH1 Signaling Pathway Through E-Proteins in Endometriotic Lesions.The Journal of clinical endocrinology and metabolism · 2020Article
- Sonic Hedgehog as a Regulator of Endometrial Mesenchymal Stem/Stromal Cell Activity.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- CXCR4 or CXCR7 antagonists treat endometriosis by reducing bone marrow cell trafficking.Journal of cellular and molecular medicine · 2020Article
- Dysregulation of miR-202-3p Affects Migration and Invasion of Endometrial Stromal Cells in Endometriosis via Targeting ROCK1.Reproductive sciences (Thousand Oaks, Calif.) · 2020Article
- GLI1 is increased in ovarian endometriosis and regulates migration, invasion and proliferation of human endometrial stromal cells in endometriosis.Annals of translational medicine · 2019Article
- Notch-1 Signaling Activation and Progesterone Receptor Expression in Ectopic Lesions of Women With Endometriosis.Journal of the Endocrine Society · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Endometriosis, a steroid hormone-dependent disease characterized by aberrant activation of estrogen receptor signaling and progesterone resistance, remains intractable because of the complexity of the pathways underlying its manifestation. We previously showed that eutopic endometria of women with endometriosis exhibit lower expression of Krüppel-like factor 9 (KLF9), a progesterone receptor coregulator in the uterus, relative to that of women without disease. Here we examined whether loss of endometrial KLF9 expression causes ectopic lesion establishment using syngeneic wild-type (WT) mice as recipients of endometrial fragments from WT and Klf9 null donors. We found significantly higher incidence of ectopic lesions with Klf9 null than WT endometria 8 weeks after tissue injection into the intraperitoneal cavity. The increased incidence of lesion establishment with Klf9 null endometria was associated with a higher expression ratio of estrogen receptor 2 isoform relative to that of estrogen receptor 1 and attenuated progesterone receptor levels in endometriotic stromal cells. PCR array analyses of Notch and Hedgehog signaling components in ectopic lesions demonstrated up-regulated expression of select genes (Jag 2, Shh, Gli1, and Stil 1) in Klf9 null lesions relative to that in WT lesions. Immunohistochemical analyses showed increased levels of Notch intracellular domain and Sonic Hedgehog proteins in Klf9 null lesions relative to that in WT lesions, confirming pathway activation. WT recipients with Klf9 null lesions displayed lower systemic levels of TNFα and IL-6 and higher soluble TNF receptor 1 than corresponding recipients with WT lesions. Our results suggest that endometrial KLF9 deficiency promotes endometriotic lesion establishment by the coincident deregulation of Notch-, Hedgehog-, and steroid receptor-regulated pathways.
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.