ArticleNephrology (Carlton, Vic.)2020
Smad3 signalling affects high glucose-induced podocyte injury via regulation of the cytoskeletal protein transgelin.
Article in Nephrology (Carlton, Vic.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Approach to Studies on Podocyte Lesions Mediated by Hyperglycemia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- [Inhibition of miR-30d-5p promotes mitochondrial autophagy and alleviates high glucose-induced injury in podocytes].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Article
- Astragaloside IV ameliorates diabetic nephropathy inInternational journal of molecular medicine · 2021Article
- miR299a-5p promotes renal fibrosis by suppressing the antifibrotic actions of follistatin.Scientific reports · 2021Article
- Bioinformatic Reconstruction and Analysis of Gene Networks Related to Glucose Variability in Diabetes and Its Complications.International journal of molecular sciences · 2020Article
- Smad3 signalling affects high glucose-induced podocyte injury via regulation of the cytoskeletal protein transgelin.Nephrology (Carlton, Vic.) · 2020Article
- The Rab-Rabphilin system in injured human podocytes stressed by glucose overload and angiotensin II.American journal of physiology. Renal physiology · 2020Article
- Long non-coding RNA cancer susceptibility candidate 2 (CASC2) alleviates the high glucose-induced injury of CIHP-1 cells via regulating miR-9-5p/PPARγ axis in diabetes nephropathy.Diabetology & metabolic syndrome · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
aimThe aim of the present study was to characterize the role of Smad3 signalling on high glucose-induced podocyte injury.
methodsSynchronized conditionally immortalized mouse podocyte cell line (MPC5) cells were treated with either D-glucose alone or D-glucose plus the Smad3 inhibitor SIS3. The distribution of F-actin and transgelin in a high glucose-induced model of podocyte injury were examined by immunofluorescence. Levels of transgelin and Smad3 signalling proteins in MPC5 cells were determined by Western blot.
resultsA disordered distribution of F-actin, as well as co-localization of F-actin and transgelin, was observed in podocytes exposed to high glucose. Increased levels of transgelin were first observed 10 minutes after treatment with glucose, suggesting that this protein is sensitive to hyperglycaemic injury. Levels of phosphorylated Smad3 and cleaved caspase 3 increased significantly with glucose stimulation. Moreover, expression of the downstream protein c-Myc, but not JAK1/STAT3, was induced in conditions of high glucose. The Smad3-specific inhibitor SIS3 prevented the effects of high glucose on Smad3 phosphorylation, expression of transgelin and c-Myc, caspase 3 cleavage and cytoskeletal organization. Expression of the tumour suppressor protein p15
conclusionSmad3 signalling plays a critical role in the modulation of hyperglycaemic injury. Targeted inhibition of the Smad3 pathway may offer a novel route for treatment of podocyte damage, especially in cases of diabetic nephropathy.
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.