Evidence map›Paper›PMID 30612136›Full record

ArticleDiabetologia2019

lncRNA H19 prevents endothelial-mesenchymal transition in diabetic retinopathy.

Anu A Thomas, Saumik Biswas, Biao Feng, Shali Chen, John Gonder, Subrata Chakrabarti

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
10.2field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

124 citing papers in PubMed, 226 citations in OpenAlex.

  1. Article
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  4. Long Noncoding RNAs as Blood-Based Biomarkers of Diabetic Retinopathy.Translational vision science & technology · 2026
    Article
  5. Article
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  7. Review
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  10. Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
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  15. Article
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64 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Anu A ThomasDepartment of Pathology and Laboratory Medicine, Western University, Dental Science Building 4033, 1151 Richmond Street, London, ON, N6A 5C1, Canada.
Saumik BiswasDepartment of Pathology and Laboratory Medicine, Western University, Dental Science Building 4033, 1151 Richmond Street, London, ON, N6A 5C1, Canada.
Biao FengDepartment of Pathology and Laboratory Medicine, Western University, Dental Science Building 4033, 1151 Richmond Street, London, ON, N6A 5C1, Canada.
Shali ChenDepartment of Pathology and Laboratory Medicine, Western University, Dental Science Building 4033, 1151 Richmond Street, London, ON, N6A 5C1, Canada.
John GonderDepartment of Ophthalmology, Western University, London, ON, Canada.
Subrata ChakrabartiDepartment of Pathology and Laboratory Medicine, Western University, Dental Science Building 4033, 1151 Richmond Street, London, ON, N6A 5C1, Canada. subrata.chakrabarti@lhsc.on.ca.
Western University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisThe pathophysiology of diabetic retinopathy is linked to hyperglycaemia and its effect on retinal microvascular tissues. The resulting endothelial injury changes the endothelial cell phenotype to acquire mesenchymal properties (i.e. endothelial-mesenchymal transition [EndMT]). Such changes can be regulated by epigenetic mechanisms, including long non-coding RNAs (lncRNAs). lncRNA H19 may influence EndMT through TGF-β. We investigated the role of H19 in regulating EndMT during diabetic retinopathy.

methodsH19 was overexpressed or silenced in human retinal endothelial cells exposed to various glucose levels. The cells were examined for H19, endothelial and mesenchymal markers. We then expanded the study to retinal tissues in a mouse model of diabetic retinopathy and also examined vitreous humour samples from individuals with proliferative diabetic retinopathy.

resultsExpression of H19 was downregulated in high glucose conditions (25 mmol/l). H19 overexpression prevented glucose-induced EndMT. Such changes appear to involve TGF-β through a Smad-independent mechanism. Diabetes caused downregulation of retinal H19. Using H19 knockout mice, we demonstrated similar EndMT in the retina. Examination of vitreous humour from individuals with proliferative diabetic retinopathy also reinforced the downregulation of H19 in diabetes. CONCLUSIONS/

interpretationWe therefore concluded that H19 regulates EndMT in diabetic retinopathy through specific mechanisms. DATA AVAILABILITY: The results from our previous microarray can be found online using the GEO accession number GSE122189.

Indexed as

AgedAnimalsDiabetic RetinopathyDown-RegulationEndothelial CellsFemaleGlucoseHumansMaleMiceMiddle AgedRetinaRNA, Long NoncodingVitreous BodyGlucoseH19 long non-coding RNARNA, Long NoncodingDiabetic retinopathyEndothelial–mesenchymal transitionH19TGF-β

Identifiers

PMID30612136
OpenAlexW2908457616

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.