ArticleBioengineered2022
Knockdown of lncRNA TUG1 alleviates diabetic retinal vascular dysfunction through regulating miR-524-5p/FGFR2.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 13 citations in OpenAlex.
- Expression of long noncoding RNAs in peripheral blood mononuclear cells of patients with type 1 diabetes mellitus: potential biomarkers for disease onset.Archives of endocrinology and metabolism · 2025Article
- Ginsenoside Rg1 inhibits angiogenesis in diabetic retinopathy through the miR-100-3p/FBXW7/c-MYC molecular axis.Journal of diabetes investigation · 2025Article
- Diabetes and diabetic associative diseases: An overview of epigenetic regulations of TUG1.Saudi journal of biological sciences · 2024Review
- Long Non-coding RNA SPAG5-AS1 Attenuates Diabetic Retinal Vascular Dysfunction by Inhibiting Human Retinal Microvascular Endothelial Cell Proliferation, Migration, and Tube Formation by Regulating the MicroRNA-1224-5p/IRS-1 Axis.Molecular biotechnology · 2023Article
- Diabetic Retinopathy: Are lncRNAs New Molecular Players and Targets?Antioxidants (Basel, Switzerland) · 2022Review
- Sprouty-related proteins with EVH1 domain (SPRED2) prevents high-glucose induced endothelial-mesenchymal transition and endothelial injury by suppressing MAPK activation.Bioengineered · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long noncoding RNAs (LncRNAs) have been shown to play critical roles in the development of diabetic retinopathy (DR), which is often regarded as the most frequent cause of visual loss in the world. This study investigated the effect and mechanism of lncRNA taurine-upregulated gene 1 (TUG1) in DR. Quantitative real-time polymerase chain reaction (qRT-PCR) revealed that TUG1 was upregulated in streptozotocin (STZ)-induced rat model of DR and human retinal microvascular endothelial cells (hRMECs) incubated with high glucose (HG). TUG1 suppression decreased the proliferation, migration, and angiogenesis of HG-induced hRMECs. TUG1 sponges miR-524-5p, which is downregulated in hyperglycemia. Additionally, the fibroblast growth factor receptor 2 (FGFR2) was verified as a miR-524-5p target gene and was overexpressed in HG-treated hRMECs. More notably, overexpression of FGFR2 has been shown to significantly reduce the impact of miR-524-5p overexpression. Additionally, TUG1 silencing ameliorates diabetes mellitus-induced retinal vascular impairment in vivo. Taken together, suppressing TUG1 impairs vascular function in diabetic retinas via controlling miR-524-5p and FGFR2, suggesting a possible therapy method for DR.
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.