ArticleHereditas2025
CD248, targeted by veratramine and neobavaisoflavone, mediates pathological changes of renal tubular epithelial cells induced by high glucose.
Article in Hereditas, 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.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundEpithelial-mesenchymal transition (EMT) of tubular epithelial cells are one of the major pathological changes of diabetic nephropathy (DN). Cluster of differentiation 248 (CD248) has been reported to be associated with fibrosis after kidney injury. The aim of this study was to investigate the mechanism of CD248 in DN and its targeted compounds. MATERIALS AND
methodsVirtual screening, molecular docking and Cellular thermal shift assays were used to explore potential small molecule compounds targeting CD248. In vitro DN model was established by treating human proximal renal tubular epithelial cell line HK-2 with high glucose (HG), and db/db mice were used as the animal model. siRNA transfection was used to knockdown CD248 in HK-2 cells, and HK-2 cells and the animals were treated with veratramine (VER) or neobavaisoflavone (NBIF). qPCR was used to detect the mRNA expression of CD248, tumor necrosis factor-α (TNF-α), interleukin (IL)-6 (IL-6), and IL-1β. Western blot was used to assess protein expression level of CD248, EMT-associated proteins, fibrosis markers, and TGF-β1/Smads pathway-associated proteins. CCK-8 assay and flow cytometry were used to detect cell viability and apoptosis, respectively. Histopathological and various biochemical indicators were used to assess renal injury in animals.
resultsCD248 was significantly up-regulated in HG-induced HK-2 cells. CD248 knockdown inhibited HG-induced cell proliferation inhibition, apoptosis and inflammatory response. HG stimulation significantly reduced the protein expression level of E-cadherin in HK-2 cells, and increased the expression levels of vimentin, α-smooth muscle actin (α-SMA), collagen I, collagen IV, fibronectin, TGF-β1, p-Smad2, p-Smad3, and Smad4, while CD248 knockdown reversed these effects. In addition, VER and neobavaisoflavone were found to bind with CD248, and they inhibited HG-induced apoptosis, inflammation, EMT and extracellular matrix synthesis in HK-2 cells, and ameliorate the renal injury of db/db mice. VER and NBIF also inhibited HG-induced activation of TGF-β1/Smads axis.
conclusionCD248 participates in HG-induced EMT of renal tubular epithelial cells and renal fibrosis by regulating TGF-β1/Smads pathway, and VER and NBIF are two potential natural drugs which targets it to ameliorate DN.
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.