ArticleKidney3602026
The Positive Feedback Loop of Hypoxia-Inducible Factor-1 α /miR-295/Factor Inhibiting Hypoxia-Inducible Factor-1 in Hyperuricemic Nephropathy.
Article in Kidney360, 2026. 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.
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
key pointsHypoxia-inducible factor-1 α -mediated induction of miR-295 in renal tubular cells in hyperuricemic nephropathy. This study reveals a hypoxia-inducible factor-1 α /miR-295/factor inhibiting hypoxia-inducible factor-1 positive feedback loop that regulates tubular damage and fibrosis in hyperuricemic nephropathy.
backgroundHyperuricemia is a common metabolic disorder and a risk factor for multiple diseases, including CKD. Hyperuricemic nephropathy (HN) affects many individuals with hyperuricemia, yet its molecular mechanisms are not fully understood, and effective treatments are lacking.
methodsIn vitro , human tubular epithelial cells (HK-2) were exposed to uric acid for 36 hours, followed by transfection with microRNA mimic or factor inhibiting hypoxia-inducible factor-1 (FIH-1) siRNA. In vivo , HN was induced in mice using potassium oxonate and adenine for 2 weeks. miR-295 mimic or anti-miR-295 was administered through tail vein injection, and mice were euthanized for analysis.
resultsWe demonstrated a significant increase of miR-295 in renal tubular cells in HN mice. Hyperuricemia led to the activation of hypoxia inducible factor-1 α (HIF-1 α ), and inhibition of HIF-1 α by YC-1 (a HIF-1 α inhibitor) prevented the increase of miR-295. Chromatin immunoprecipitation assay further verified HIF-1 α binding to the miR-295 gene promoter directly. Functionally, inhibition of miR-295 led to increased cell death and tubulointerstitial fibrosis in HN mice, whereas supplementation of miR-295 mimic had kidney-protective effects in this model. miR-295 suppressed the expression of FIH-1) in both in vitro and in vivo models of HN. Luciferase microRNA target reporter assay further verified FIH-1 as a direct target of miR-295. In addition, knockdown of FIH-1 inhibits tubular cell apoptosis and profibrotic cytokines production in HK2 cells during uric acid treatment.
conclusionsThis study reveals a HIF-1 α /miR-295/FIH-1 positive feedback loop that regulates tubular damage and fibrosis in HN.
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.