ArticleAnimal cells and systems2020
miR-122 promotes diabetic retinopathy through targeting TIMP3.
Article in Animal cells and systems, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- MiRNAs in hyperglycemia-induced metabolic memory: established mechanisms and emerging nuclear activation concepts.Diabetology & metabolic syndrome · 2026Review
- The role of serum miR-28-5p in predicting diabetic retinopathy onset in type 2 diabetes.BMC endocrine disorders · 2026Article
- miR-106a-5p targets CREB1 to regulate the inflammatory response in diabetic retinopathy.BMC ophthalmology · 2025Article
- miR-130a-3p enhances autophagy through the YY1/PI3K/AKT/mTOR signaling pathway to regulate macrophage polarization and alleviate diabetic retinopathy.Journal of diabetes investigation · 2025Article
- Role of miRNA‑122 in cancer (Review).International journal of oncology · 2024Review
- Mechanistic and therapeutic perspectives of non-coding RNA-modulated apoptotic signaling in diabetic retinopathy.Cell biology and toxicology · 2024Review
- Noncoding RNAs Are Promising Therapeutic Targets for Diabetic Retinopathy: An Updated Review (2017-2022).Biomolecules · 2022Review
- Decreased Levels of miR-126 and miR-132 in Plasma and Vitreous Humor of Non-Proliferative Diabetic Retinopathy Among Subjects with Type-2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Ameliorating Potential of Quercetin and Curcumin on Glucose-6-Phosphate Dehydrogenase ExpressionAvicenna journal of medical biotechnologyArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic retinopathy (DR) is a primary complication of diabetes mellitus. DR can cause severe vision loss for patients. miR-122 is elevated in DR patients, while its role in DR is unclear. Hence, the purpose of this study was to analyze the effect of miR-122 on the function of high glucose-induced REC cells and the underlying molecular mechanisms. In this study, our results revealed that miR-122 was up-regulated in high glucose-induced human retinal pigment epithelial cells (ARPE-19). High glucose decreased the cell viability of ARPE-19 cells, which was then restored by miR-122 knockdown. In addition, miR-122 knockdown suppressed apoptosis of high glucose-induced ARPE-19 cells. High glucose also inhibited B-cell lymphoma-2 (Bcl-2) level and increased cleaved caspase-3 level in ARPE-19 cells, which were reversed by miR-122 knockdown. Tissue inhibitor of metalloproteinases-3 (TIMP3) was a direct target of miR-122. TIMP3 was decreased in high glucose-induced ARPE-19 cells, and the decrease was abrogated by miR-122 knockdown. In addition, the effects of miR-122 overexpression in cell viability and apoptosis of high glucose-induced ARPE-19 were abolished by overexpression of TIMP3. In conclusion, the effect and mechanism of miR-122 on high glucose-induced ARPE-19 cells were demonstrated for the first time. miR-122 promoted diabetic retinopathy through targeting TIMP3, making miR-122 a promising target for diabetic retinopathy therapy.
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