ArticleBioengineered2022
Trimetazidine mitigates high glucose-induced retinal endothelial dysfunction by inhibiting PI3K/Akt/mTOR pathway-mediated autophagy.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Potential Mechanisms of Trimetazidine and Coenzyme Q10 Against Antipsychotic-Induced Myocarditis: A Network Pharmacology, Molecular Docking, and Molecular Dynamics Simulation Study.CNS neuroscience & therapeutics · 2026Article
- Trimetazidine modulates angiogenesis, inflammation, and metabolism-related gene expression to promote diabetic foot ulcer healing: a transcriptomic analysis.Pharmacological reports : PR · 2026Article
- Ginsenoside Rg1 alleviates HG-induced autophagy of retinal microvascular endothelial cells by activating ACE2/Ang1-7/Mas in vitro.Scientific reports · 2025Article
- Article
- 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
- BECLIN-1/BECN1 at the barrier: a gatekeeper of epithelial and endothelial homeostasis.Autophagy reports · 2025Review
- METTL3 blocked the progression of diabetic retinopathy through m6A-modified SOX2.Open medicine (Warsaw, Poland) · 2025Article
- Heyingwuzi formulation alleviates diabetic retinopathy by promoting mitophagyWorld journal of diabetes · 2024Article
- Role of Trimetazidine in Ameliorating Endothelial Dysfunction: A Review.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Ghrelin inhibits autophagy mediated by AKT/mTOR pathway to ameliorate retinal angiogenesis induced by high glucose stress.International journal of ophthalmology · 2024Article
- Mechanistic insights into the alterations and regulation of the AKT signaling pathway in diabetic retinopathy.Cell death discovery · 2023Review
- Regulatory effects of trimetazidine in cardiac ischemia/reperfusion injury.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- Preparation of Ultra-Small Copper Nanoparticles-Loaded Self-Healing Hydrogels with Antibacterial, Inflammation-Suppressing and Angiogenesis-Enhancing Properties for Promoting Diabetic Wound Healing.International journal of nanomedicine · 2023Article
- Long term high glucose exposure induces premature senescence in retinal endothelial cells.Frontiers in physiology · 2022Article
- Erythropoietin Activates Autophagy to Regulate Apoptosis and Angiogenesis of Periodontal Ligament Stem Cells via the Akt/ERK1/2/BAD Signaling Pathway under Inflammatory Microenvironment.Stem cells international · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trimetazidine (TMZ), as a metabolic regulator, has been widely testified to exhibit positive therapeutic effects on various disease models, but its role in diabetic retinopathy has not been reported. Therefore, this study was designed with the purpose of exploring the effects of TMZ on high-glucose (HG)-induced retinal endothelial dysfunction and its underlying mechanism. To establish DR model in vitro, 30 mM glucose was applied to induce human retinal endothelial cells (HRECs). Cell proliferation, invasion, and migration were examined by means of Cell Counting Kit-8, transwell, and wound healing assays, respectively. The tubule formation experiment was used to test the tubulogenesis ability and fluorescein isothiocyanate (FITC)-albumin was utilized to measure the permeability of monolayer HRECs. In addition, immunofluorescence and Western blot were employed to detect protein expression. Compared with the HG-induced group, TMZ concentration dependently inhibited the proliferation, migration, and angiogenesis of HG-induced HRECs, decreased the permeability of monolayer HRECs, and increased the protein expression levels of Claudin-5 and VE-cadherin. In addition, TMZ intervention increased the expression of p-PI3K, p-AKT, and p-mTOR but decreased the expression of LC3I, LC3II, and Beclin 1, which were then partially reversed by P13 K inhibitor (LY294002). Moreover, the autophagy agonist rapamycin (RAPA) was also testified to reverse the inhibitory effects of TMZ on the proliferation, migration, and angiogenesis of HG-induced HRECs. In summary, TMZ inhibited excessive autophagy by activating PI3K/Akt/mTOR pathway, thereby improving retinal endothelial dysfunction induced by HG.
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