ArticleRSC advances2019
Retracted Article: Long non-coding RNA TUG1 alleviates high glucose induced podocyte inflammation, fibrosis and apoptosis in diabetic nephropathy
Article in RSC advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 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
5 citing papers in PubMed, 5 citations in OpenAlex.
- Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy.Current molecular medicine · 2025Review
- Diabetes and diabetic associative diseases: An overview of epigenetic regulations of TUG1.Saudi journal of biological sciences · 2024Review
- Long non-coding RNA TUG1 sponges microRNA-9 to protect podocytes from high glucose-induced apoptosis and mitochondrial dysfunction via SIRT1 upregulation.Experimental and therapeutic medicine · 2022Article
- Review
- Differential Expression of Serum TUG1, LINC00657, miR-9, and miR-106a in Diabetic Patients With and Without Ischemic Stroke.Frontiers in molecular biosciences · 2021Article
Corrections and comments
- Retracted
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is the most common cause of end-stage renal disease (ESRD) in developed countries. The long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) is associated with mitochondrial function in podocytes in DN. However, the detailed mechanism of TUG1 in DN has not yet been fully elucidated. In this study, we found that the expression levels of TUG1 and E2F transcription factor 3 (E2F3) were downregulated, and microRNA-27a-3p (miR-27a-3p) level was upregulated in DN tissues and HG-treated podocytes. Function analysis indicated that TUG1 overexpression inhibited inflammation, fibrosis and apoptosis in HG-induced podocytes. Rescue experiments demonstrated that miR-27a-3p reversed the suppression effects of TUG1 on apoptosis, fibrosis and inflammation in HG-stimulated podocytes, while E2F3 abrogated the promotion effects of miR-27a-3p on apoptosis, fibrosis and inflammation in HG-induced podocytes. Mechanical analysis revealed that TUG1 regulated E2F3 expression
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.