ArticleScientific reports2025
USP37-stabilized SALL4 promotes the keloid formation by PI3K/AKT pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Mitochondrial mGPDH Modulates Fibroblast Function in Diabetic Wound Healing via the SIRT1-c-Myc-TGF-β1 Axis.Diabetes · 2026Article
- Trichinella spiralis serine protease mediates larval invasion of gut epithelium via binding to CK8 and activating RhoA/ROCK1 pathway.PLoS neglected tropical diseases · 2025Article
- The PI3K/AKT/mTOR pathway in scar remodeling and keloid formation: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 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
7 authors.
Funding
Abstract
Spalt-like transcription factor 4 (SALL4) plays a vital role in the progression of many human diseases. However, the role and mechanism of SALL4 regulates in keloid formation remain unclear. The mRNA levels of SALL4 and ubiquitin-specific peptidase 37 (USP37) in keloid tissues and keloid fibroblasts were determined by quantitative real-time PCR. Western blot was performed to measure the protein levels of SALL4, USP4/10/37, collagen-related markers, and PI3K/AKT-related markers. The growth, invasion and migration of keloid fibroblasts were determined using CCK8 assay, EdU assay, flow cytometry, transwell assay and wound healing assay. Cell glycolysis was assessed by detecting glucose consumption and lactate production. The interaction between USP37 and SALL4 was confirmed by co-immunoprecipitation assay. SALL4 had increased expression in keloid tissues and keloid fibroblasts. Silencing of SALL4 inhibited the growth, invasion, migration, extracellular matrix (ECM) accumulate and glycolysis of keloid fibroblast, while its overexpression had the opposite effects. In terms of mechanism, USP37 stabilized SALL4 expression through deubiquitinating. Functional experiments suggested that SALL4 overexpression reversed the inhibitory effect of USP37 knockdown on keloid fibroblast functions. Moreover, USP37/SALL4 axis could increase the activity of PI3K/AKT pathway, and PI3K pathway inhibitor LY294002 abolished SALL4-mediated the promoting on keloid fibroblast functions. USP37-activated SALL4 might enhance keloid fibroblast growth, invasion, migration, ECM accumulation and glycolysis via activating PI3K/AKT pathway.
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.