ArticleAmerican journal of translational research2021
Effects of miR-151-3p-mediated GLCCl1 expression on biological function in children with nephrotic syndrome.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed, 2 citations in OpenAlex.
- Clinical value of miR-551b-5p in children with primary nephrotic syndrome and its regulatory role in disease progression.Hereditas · 2026Article
- miRNAs in Glomerular Diseases: From Pathogenic Insight to Therapeutic Potential: A Narrative Review.Cells · 2026Review
- MicroRNAs in idiopathic childhood nephrotic syndrome.Clinical and experimental nephrology · 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to confirm the association of miR-151-3p with nephrotic syndrome (NS) in children and to explore the molecular mechanisms by which glucocorticoid-induced transcript 1 gene (GLCCI1) targets cellular biological functions in children with nephrotic syndrome.
methodsmiR-151-3p levels were detected in 20 children with hormone-sensitive nephrotic syndrome (SSNS), 15 children with steroid-dependent nephrotic syndrome (SDNS) and 20 children with steroid-resistant nephrotic syndrome (SRNS), using qRT-PCR before and after glucocorticoid treatment, and TargetScan information software was used to predict the biological targets between miR-151-3p and GLCCI1 gene. The change in albumin-to-creatinine ratio (ACR) before and after treatment in children with NS was determined to judge the treatment efficacy.
resultsCompared with healthy controls, pediatric patients with NS had significantly increased serum miR-151-3p levels before treatment (P<0.01). After glucocorticoid treatment, children with SSNS/SDNS had significantly decreased serum miR-151-3p levels (P<0.01), with no significant difference from healthy controls. The ACR of children with SSNS/SDNS was significantly lower than that before treatment (P<0.05), and the symptoms of proteinuria were significantly relieved. The serum miR-151-3p levels and ACR of children with SRNS did not change significantly from that before treatment (P>0.05), and the symptoms of proteinuria were also not improved. Targetscan prediction results showed that miR-151-3p has well-matched sites with GLCCI13'UTR.
conclusionmiR-151-3p directly influences the onset and progression of NS through targeted regulation of GLCCI1 expression in podocytes. miR-151-3p may be a biological marker for the diagnosis, treatment and prognosis of NS.
Indexed as
Identifiers
33841701PMC8014414W3155540685What 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.