ArticleBMC women's health2025
Role of SMOC2 in adenomyosis: implications for ECM remodeling and EMT pathogenesis.
Article in BMC women's health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The endometriosis-adenomyosis spectrum: shared pathophysiology and microenvironment-driven disease divergence.Reproductive biology and endocrinology : RB&E · 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
backgroundAdenomyosis is a common gynecological disorder characterized by the invasion of endometrial tissue into the myometrium, resulting in severe dysmenorrhea and menorrhagia. This study aimed to explore the role of SMOC2 (SPARC related modular calcium binding 2), an extracellular matrix (ECM) -associated protein, in the pathogenesis of adenomyosis and its potential as a therapeutic target.
methodsWe conducted a clinical study involving 35 patients diagnosed with adenomyosis and 30 controls. Ectopic endometrial tissue samples were collected and analyzed using immunohistochemistry (IHC), Masson staining, and cell culture techniques. The proliferative effect of SMOC2 on cells was evaluated using CCK- 8 assay, while the expression of SMOC2 and epithelial-mesenchymal transition (EMT) was assessed using real-time PCR and western blot analysis.
resultsSMOC2 expression was significantly higher in the ectopic endometrial tissue of adenomyosis patients compared to controls. SMOC2 could promote cell proliferation. Overexpression of SMOC2 significantly upregulated mesenchymal markers N-cadherin and α-SMA, and downregulated epithelial marker E-cadherin. Conversely, knocking down SMOC2 with siRNA reversed these effects. These findings indicate that SMOC2 promotes EMT in adenomyotic stromal cells. Additionally, SMOC2 also activated the MMP9 signaling pathway, which plays a crucial role in the extracellular matrix (ECM) remodeling.
conclusionsSMOC2 appears to be a key regulator in the pathogenesis of adenomyosis, promoting ECM remodeling and EMT, both of which are characteristic of the disease. Targeting SMOC2 may provide a novel therapeutic strategy for the treatment of adenomyosis.
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.