ArticleCurrent pharmaceutical biotechnology2026
Estradiol Promotes Endometriosis Progression
Article in Current pharmaceutical biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- The importance of gene polymorphism in familial inheritance of endometriosis.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2026Article
- Molecular mechanisms underlying the inhibition of cell migration and invasion in endometriosis: Advances in pharmacological research (Review).Biomedical reports · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
aimsThe present study aimed to examine the roles of circRNA-circSMAD2 and its regulatory mechanisms in endometriosis (EMs).
backgroundEvidence has confirmed that circRNAs play multiple roles in regulating the occurrence and development of EMs, but the regulatory mechanisms of circRNAs in EMs remain largely unknown.
objectivesThe roles and regulatory mechanisms of circSMAD2 in EMs.
methodsEutopic and ectopic endometrium of ovarian EMs as well as normal endometrial tissues, were used to extract circRNA, mRNA, and total proteins. The human endometrial stromal cell lines (ThESCs) and endometrial stromal cells (ESCs) were stimulated with different concentrations or times of 17β-estradiol (E2). The mouse model of EMs was established by implanting uterine horns onto the peritoneum wall using a suture.
resultsCompared with normal tissues, the expression of circSMAD2 was significantly decreased in eutopic and ectopic endometrial tissues. Furthermore, the expression of circSMAD2 was downregulated by E2 in a dose- and time-dependent manner in ThESCs and ESCs. Overexpression of circSMAD2 inhibited the invasion and migration of ThESCs, while knockdown of circSMAD2 exerted the opposite effect. The RNA binding protein quaking (QKI), which is involved in circRNA formation, was lower in eutopic and ectopic endometrial tissues compared to normal tissues. Moreover, E2 suppressed the expression of circSMAD2 by inhibiting the expression of QKI. Additionally, E2 enabled the expression of estrogen receptor beta (ERβ) to inhibit the expression of QKI and circSMAD2 in vitro and in vivo.
conclusionThe E2/ERβ/QKI/circSMAD2 pathway was involved in cellular migration and invasion in EMs.
Indexed as
Identifiers
39980288What 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.