ArticleHereditas2025
MiR-106b-5p improving the progression of chronic kidney disease by inhibiting the TGF-β/Smad pathway.
Article in Hereditas, 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.
- Circ-PRKCI attenuates acute lung injury secondary to sepsis by targeting the miR-106b-5p/GAB1 axis.European journal of medical research · 2026Article
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
backgroundChronic Kidney Disease (CKD) is a progressive disorder marked by renal impairment and declining kidney function.
aimsTo investigate the expression of miR-106b-5p in CKD and its regulatory relationship with the TGF-β/Smad pathway.
methodsA total of 150 cases of CKD patients were selected as the observation group, while 100 healthy individuals served as the control group. Lipopolysaccharide (LPS) was utilized to induce damage to HK-2 cells. Real-time fluorescence PCR was used to detect the expression of genes. The CCK - 8 assay was utilized to evaluate cell proliferation, while flow cytometry was applied to measure the cell apoptosis rate.
resultsmiR-106b-5p is notably downregulated in CKD and exhibits a significant positive correlation with the eGFR in affected patients. Additionally, miR-106b-5p demonstrates a strong association with the levels of inflammatory factors in individuals with CKD. Furthermore, the expression of miR-106b-5p is reduced in LPS-induced HK-2 cells. Upregulation of miR-106b-5p can improve the inhibitory effect of LPS on the viability of HK-2 cells, reduce the apoptosis rate of cells, and alleviate the inflammatory response. miR-106b-5p serves as a negative regulatory factor within the TGF-β/Smad signaling pathway by directly targeting the pivotal receptor TGFBR2 and the downstream effectors SMAD2/3 within the TGF-β signaling cascade.
conclusionsmiR-106b-5p ameliorates CKD progression by suppressing the TGF - β/Smad signaling pathway and could potentially be a therapeutic target for CKD.
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.