ArticleInternational urology and nephrology2025
Aldosterone promotes calcification of vascular smooth muscle cells in mice through the AIF-1/Wnt/β-catenin signaling pathway.
Article in International urology and nephrology, 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.
- Tempol Mitigates Methotrexate-Induced Osteotoxicity via Oxidative Stress Modulation and MAPK Pathway Inhibition.Drug design, development and therapy · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
objectiveThis study aimed to investigate the impact of aldosterone on calcification in murine vascular smooth muscle cells (VSMCs) via the allograft inflammatory factor-1 (AIF-1)/Wnt/β-catenin signaling pathway.
methodsMouse VSMCs were cultured in vitro, and calcification was induced by treatment with 100 nM aldosterone. The level of calcification in mouse VSMCs was evaluated using colorimetric assays to assess ALP activity and qRT-PCR to identify the expression of calcification-related markers, such as Runx2, α-SMA, OCN, and ALP mRNA. Western blot analysis was performed to determine the protein expression levels associated with the Wnt/β-catenin pathway (LRP6, p-LRP6, GSK3β, p-GSK3β, β-catenin) and AIF-1. Plasmid transfection techniques were utilized to either knock down or overexpress AIF-1, and the subsequent alterations in these markers were observed.
results(1) Compared to the control group, the aldosterone treatment group with exhibited a significant increase in ALP. Concurrently, Runx2, OCN, and ALP mRNA levels increased, as did LRP6, p-LRP6, GSK3β, p-GSK3β, β-catenin, and AIF-1 protein levels. Additionally, a significant decrease in the expression of α-SMA mRNA was observed (P < 0.05). (2) The aldosterone + oe-AIF-1 group showed significant increases in ALP activity compared to the aldosterone + oe-NC group, whereas the aldosterone + sh-AIF-1 group showed significant decreases (P < 0.05). (3) The aldosterone + oe-AIF-1 group exhibited significantly upregulated expression of AIF-1, p-LRP6/LRP6, p-GSK3β/GSK3β, and β-catenin proteins relative to the aldosterone + oe-NC group (P < 0.05). This was concurrent with increased mRNA expression of Runx2, OCN, and ALP, and decreased α-SMA mRNA expression (P < 0.05).
conclusionAldosterone affects the calcification process in mouse VSMCs, and the activation of the AIF-1/Wnt/β-catenin signaling pathway is the mechanism behind its action.
Indexed as
Identifiers
39312016What 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.