ArticleActa Cardiologica Sinica2025
IGF2BP1-Mediates m
Article in Acta Cardiologica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
No grant is acknowledged in the PubMed record.
Abstract
Background: Atherosclerosis accelerates the progression of diabetes and metabolic syndrome. Endothelial to mesenchymal transition (EndMT) has been reported to promote the development of atherosclerosis and the generation of extracellular matrix. However, the mechanism of EndMT in diabetic atherosclerosis has not been fully clarified. Methods: Human umbilical vein endothelial cells (HUVECs) were treated with high glucose (HG) and transforming growth factor beta 1 (TGF-β1) to induce EndMT. The levels of insulin-like growth factor 2 mRNA-binding protein (IGF2BP), Krüppel-like factor 4 (KLF4), Adhesion-regulating molecule 1 (ADRM1), CD31, vWF, α-SMA and vimentin were detected by qRT-PCR and Western blot. Correlations among IGF2BP1, KLF4 and ADRM1 were analyzed by RIP and ChIP assays. MeRIP-qPCR was used to detect the m Results: IGF2BP1, KLF4 and ADRM1 were upregulated in the diabetic atherosclerosis cell model, and IGF2BP1 knockdown inhibited HG combined with TGF-β1-induced EndMT in HUVECs. Mechanically, IGF2BP1 regulated the m Conclusions: This study demonstrated that IGF2BP1-mediated m
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.