ArticleArchives of pharmacal research2021
miR-139-5p promotes neovascularization in diabetic retinopathy by regulating the phosphatase and tensin homolog.
Article in Archives of pharmacal research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 17 citations in OpenAlex.
- Circular RNA circPSEN1 promotes neovascularization by regulating the miR-150-5p/TRIM65 axis in diabetic retinopathy.Biochemistry and biophysics reports · 2026Article
- hsa_circ_0068631 facilitates the progression of diabetic retinopathy via regulating miR-140-5p in retinal microvascular endothelial cells.BMC ophthalmology · 2026Article
- Decreased miR-455-3p promotes diabetic retinopathy progression via modulating retinal endothelial proliferation and apoptosis.BMC ophthalmology · 2025Article
- Type 2 Diabetes Induces Mitochondrial Dysfunction in Zebrafish Skeletal Muscle Leading to Diabetic Myopathy via the miR-139-5p/NAMPT Pathway.International journal of molecular sciences · 2025Article
- Targeting microRNAs in diabetic retinopathy: from pathogenic mechanisms to therapeutic potentials.Frontiers in endocrinology · 2025Review
- miR-16-5p Regulates Proliferation and Apoptosis in High Glucose-Treated Human Retinal Microvascular Endothelial Cells by Targeting VEGFA and TGFBR1.Journal of ophthalmology · 2025Article
- Article
- Advances in Research Related to MicroRNA for Diabetic Retinopathy.Journal of diabetes research · 2024Review
- The Potential Role of MiRs-139-5p and -454-3p in Endoglin-Knockdown-Induced Angiogenic Dysfunction in HUVECs.International journal of molecular sciences · 2023Article
- Circ VRK1/microRNA-17/PTEN axis modulates the angiogenesis of human brain microvascular endothelial cells to affect injury induced by oxygen-glucose deprivation/reperfusion.BMC neuroscience · 2023Article
- Noncoding RNAs Are Promising Therapeutic Targets for Diabetic Retinopathy: An Updated Review (2017-2022).Biomolecules · 2022Review
- miRNA signatures in diabetic retinopathy and nephropathy: delineating underlying mechanisms.Journal of physiology and biochemistry · 2022Review
- Hyaluronic Acid Facilitates Angiogenesis of Endothelial Colony Forming Cell Combining With Mesenchymal Stem CellFrontiers in bioengineering and biotechnology · 2022Article
- Downregulation of Circular RNA PSEN1 ameliorates ferroptosis of the high glucose treated retinal pigment epithelial cells via miR-200b-3p/cofilin-2 axis.Bioengineered · 2021Article
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathological retinal neovascularization is a driver of the progression of diabetic retinopathy (DR). The present study sought to identify the microRNAs (miRNAs) that are differentially expressed during the progression of DR as well as to explore the specific regulatory mechanism of those miRNAs in retinal neovascularization. Using a microarray data set and a diabetic mouse model, it was determined that miR-139-5p was significantly upregulated during the progression of DR. The in vitro investigation revealed an elevation in the miR-139-5p level in both the high glucose (HG)-treated mouse retinal microvascular endothelial cells (mRMECs) and the HG-treated human RMECs (hRMECs). The miR-139-5p overexpression elevated cell migration, facilitated tube formation, and increased vascular endothelial growth factor (VEGF) protein level in the hRMECs. While the angiogenic effect of miR-139-5p overexpression was halted by an anti-VEGF antibody. Meanwhile, the miR-139-5p knockdown eliminated the VEGF-induced cell migration and tube formation in the hRMECs. The phosphatase and tensin homolog (PTEN) was the target gene of the miR-139-5p. PTEN overexpression removed the angiogenic effect of miR-139-5p overexpression, which led to reduced cell migration and tube formation. In the diabetic mice, the miR-139-5p antagomir effectively decreased the acellular capillaries and suppressed the formation of aberrant blood vessels in the retinal tissues. Taken together, miR-139-5p promotes retinal neovascularization by repressing PTEN expression.
Indexed as
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.