ArticleMolecular biology reports2026
PTBP3 promotes diabetic nephropathy via Smad3-dependent podocyte-mesenchymal transition.
Article in Molecular biology reports, 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
backgroundDiabetic nephropathy (DN) is the leading cause of end-stage renal disease (ESRD) worldwide, yet effective therapeutic targets remain limited. Podocyte injury and podocyte to mesenchymal transition represent critical pathological events driving renal fibrosis and progressive dysfunction in DN. METHODS AND
resultsThrough integrated transcriptomic data from public databases, we discovered that the RNA-binding protein PTBP3 is aberrantly elevated in DN. PTBP3 upregulation was validated in renal tissues from streptozotocin (STZ)-induced diabetic mice and in high glucose (HG) challenged podocytes, suggesting its potential involvement in DN pathogenesis. In PTBP3 knockdown mice, STZ-induced 24 h urinary protein, serum creatinine and blood urea nitrogen were significantly attenuated. Histological analyses revealed ameliorated glomerular hypertrophy and mesangial expansion, and reduced renal fibrosis upon PTBP3 knockdown. In addition, the results showed that the PTBP3 expression in glomeruli of diabetic mice was increased and PTBP3 silencing inhibited the EMT of podocytes in diabetic mice, which was accompanied with the decreased expression of SMAD3. This was evidenced by the restored expression of E-cadherin and the reduced expression of N-cadherin, vimentin, and fibronectin. The results from culture podocytes showed similar results. Mechanistically, the dual-luciferase and RNA immunoprecipitation assays demonstrated that PTBP3 interacted with the 3'-UTR of SMAD3 mRNA to facilitate its stabilization and increase its total protein and subsequent phosphorylation levels.
conclusionsNotably, PTBP3 knockdown ameliorated renal fibrosis and preserved renal function, underscoring the therapeutic potential of targeting podocyte epithelial-mesenchymal transition in DN.
Indexed as
Identifiers
42801358What 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.