ArticleArchives of clinical and biomedical research2025
Regulation of RSPO3-LGR4 Signaling: Emerging Role in Inflammation Revealed by Network Analysis.
Article in Archives of clinical and biomedical research, 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.
- Limitations of Current Therapies and Barriers in Alzheimer's Disease.Archives of internal medicine research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
RSPO3, as a member of the R-spondin gene family, is a secreted molecule that enhances one of the fundamental biological pathways, the canonical Wnt signaling pathway. Once secreted from endothelial cells or macrophages, it typically binds to specific receptors from the LGR family. Additionally, LGR-independent activation of the Wnt cascade, driven by RSPOs, has also been described, mediated by heparan sulfate proteoglycans (HSPGs). LGR4 (GPR48) belongs to the G-protein-coupled receptor superfamily, subfamily B. It is widely recognized as an RSPO3-binding receptor and, thereafter, a Wnt signaling potentiator. Expression patterns of both RSPO3 and LGR4 have been found across various tissues. RSPO3 regulates stem cell maintenance in the intestine, in addition to its function in liver endothelial cells in terms of liver zonation or osteoblast differentiation. LGR4 has shown expression in hypothalamic neurons, regulating reproductive hormone secretion and control of food intake. Various studies reported the contribution of both RSPO3 and LGR4 to inflammatory cascades. Specifically, the RSPO3-LGR4 ligand-receptor interaction was shown to activate the NLRP3 inflammasome and β-catenin-NF-kB signaling cascade. Endothelial-derived RSPO3 exerts regenerative potential via the RSPO3-LGR4-ILK-AKT pathway, as presented
Indexed as
Identifiers
What Socratic 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 Socratic graph.