ArticleDiabetology & metabolic syndrome2026
Dysregulation of the miR-4286 in diabetic kidney disease and its role in inflammatory response.
Article in Diabetology & metabolic syndrome, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
objectiveWe aimed to investigate the expression level and diagnostic value of miR-4286 in serum of DKD patients and validate its effect on podocyte inflammatory response and apoptosis in vitro.
methodsWe detected the expression level of serum miR-4286 and CADM1 in DKD patients and healthy individuals. Clinical correlations of miR-4286 with estimated glomerular filtration rate (eGFR), urinary albumin-to-creatinine ratio (UACR), and KDIGO risk categories were analyzed. We detected the expression change of miR-4286 in podocytes treated. ROC analysis was used to evaluate the diagnostic value of miR-4286. Dual-luciferase assay and RNA immunoprecipitation (RIP) were used to validate the targeting relationship between miR-4286 and CADM1. TNF-α and IL-1β in supernatants were detected by ELISA, CADM1 protein expression was assessed by Western blotting, and apoptosis was detected by flow cytometry.
resultsIn DKD patients, upregulation of serum miR-4286 and downregulation of CADM1 were observed and negatively correlated. MiR-4286 levels were negatively correlated with eGFR, positively correlated with UACR, and increased across KDIGO risk categories. In vitro, mimicking diabetic conditions revealed that miR-4286 was upregulated and CADM1 was downregulated at both mRNA and protein levels in podocytes in HG group. Functionally, suppressing miR-4286 could ameliorate the HG-induced inflammation and apoptosis. While CADM1 knockdown aggravated both two kinds of damages. Importantly, suppressing CADM1 partly rescued the apoptosis from co-silencing miR-4286.
conclusionThis study demonstrated that miR-4286 could regulate inflammatory response and podocyte function in DKD by targeting CADM1. Upregulation of miR-4286 would suppress CADM1, further enhancing the release of inflammatory factors and apoptosis.
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.