ArticleAmerican journal of translational research2022
Klotho/FGF23 and Wnt in SHPT associated with CKD
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed, 1 citations in OpenAlex.
- MiR-29a-3p inhibits fibrosis of diabetic kidney disease in diabetic miceWorld journal of diabetes · 2025Article
- Analysis of Factors Influencing Cardiovascular Events and Mortality in Patients on Dialysis after Parathyroidectomy.Current pharmaceutical design · 2025Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveRecently, the interaction between Klotho/fibroblast growth factor 23 (FGF-23) axis and Wnt signaling has been recognized to be responsible for chronic kidney disease (CKD)-associated comorbidities, including secondary hyperparathyroidism (SHPT). This study aimed to investigate the molecular mechanism of the interaction between Klotho/FGF23 axis and Wnt.
methodsA SHPT model was successfully established with a high-phosphorus diet plus 5/6 nephrectomy. Cell counting Kit-8 (CCK-8) assay and calcium deposit experiment were applied to detect the proliferation and calcium levels. Quantitative real-time PCR (qRT-PCR), Western blotting and immunofluorescence (IF) were used to determine the expression or location of FGF23, calcification-related factors and β-catenin after lentivirus-mediated Klotho overexpression. Luciferase reporter assay was performed to further validate the transcriptional regulation between microRNA-29a (miR-29a) and Dickkopf-1 (DDK1).
resultsWe found increased serum biochemical factors including parathyroid hormone (PTH), phosphorus, calcium, enhanced parathyroid calcification, and decreased expressions of Klotho in a rat model of secondary hyperparathyroidism. Moreover, genetic-induced upregulation of Klotho inhibited the proliferation, reduced the calcification and the alkaline phosphatase (ALP) activity, and downregulated Wnt/β-catenin signaling in parathyroid cells.
conclusionsMechanistically, Klotho suppressed miR-29a expression, led to upregulated expression of Wnt/β-catenin signaling inhibitor DKK1, and finally downregulated the activity of Wnt/β-catenin signaling. These findings suggest a novel molecular mechanism in the pathogenesis of CKD-associated SHPT, which provides a potential therapeutic target in the future.
Indexed as
Identifiers
35273691PMC8902549W4226342139What 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.