ArticleAntioxidants (Basel, Switzerland)2019
MicroRNA-34a (miR-34a) Mediates Retinal Endothelial Cell Premature Senescence through Mitochondrial Dysfunction and Loss of Antioxidant Activities.
Article in Antioxidants (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Therapeutic Effects of microRNAs on Nonalcoholic Fatty Liver Disease (NAFLD) and Nonalcoholic Steatohepatitis (NASH): A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2023Pooled it
- Doxorubicin and 4-Hydroperoxycyclophosphamide Alter Mitochondrial Dynamics and miR-34 Expression in Spermatogonia and Spermatocytes In Vitro.Basic & clinical pharmacology & toxicology · 2026Article
- LiposomalInternational journal of molecular sciences · 2026Article
- MicroRNAs: A Social Network in Diabetic Retinopathy.Biomolecules · 2026Review
- Mechanisms and clinical implications of radiation-induced endothelial dysfunction.Radiation oncology (London, England) · 2026Review
- Review
- Repurposing lurasidone to alleviate doxorubicin-induced cardiotoxicity and neurotoxicity via BDNF/TrkB/PI3K/Akt/CREB and miR-34a-5p/PGC-1α pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis.Acta pharmacologica Sinica · 2026Article
- Potential influence of carbonic anhydrase 9 genetic variants and expression levels on the progression of diabetic retinopathy.International journal of medical sciences · 2026Article
- miR‑34a induces apoptosis and pyroptosis in D‑Galactose‑induced aging cochlear hair cells via inhibiting TFAM and promoting mitochondrial dysfunctionInternational journal of molecular medicine · 2025Article
- The Role of Endothelial Senescence in the Pathogenesis of Diabetic Retinopathy.International journal of molecular sciences · 2025Review
- microRNA-Mediated Regulation of Oxidative Stress in Cardiovascular Diseases.Journal of clinical laboratory analysis · 2025Review
- From fatty liver to fibrosis: the impact of miRNAs on NAFLD and NASH.Functional & integrative genomics · 2025Review
- MicroRNA-34a Mediates the Aldosterone-Induced Acceleration of Endothelial Senescence.International journal of hypertension · 2025Article
- From Microcirculation to Aging-Related Diseases: A Focus on Endothelial SIRT1.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Emerging insights into the pathogenesis and therapeutic strategies for vascular endothelial injury-associated diseases: focus on mitochondrial dysfunction.Angiogenesis · 2024Review
- The potential of therapeutic strategies targeting mitochondrial biogenesis for the treatment of insulin resistance and type 2 diabetes mellitus.Archives of pharmacal research · 2024Review
- Therapeutic targeting of cellular senescence in diabetic macular edema: preclinical and phase 1 trial results.Nature medicine · 2024Article
- Dysregulation of histone deacetylases in ocular diseases.Archives of pharmacal research · 2024Review
- Stem Cell-Derived Exosomes: Natural Intercellular Messengers with Versatile Mechanisms for the Treatment of Diabetic Retinopathy.International journal of nanomedicine · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Stress-associated premature senescence (SAPS) is involved in retinal microvascular injury and diabetic retinopathy. We have investigated the role and mode of action of miR-34a in retinal endothelial cells senescence in response to glucidic stress. Human retinal microvascular endothelial cells (HuREC) were exposed to glucidic stress (high glucose (HG) = 25 mM d-glucose) and compared to cells exposed to normal glucose (NG = 5 mM) or the osmotic control l-glucose (LG = 25 mM). HG stimulation of HuREC increased the expression of miR-34a and induced cellular senescence. HG also increased the expression of p16ink4a and p21waf1, while decreasing the histone deacetylase SIRT1. These effects were associated with diminished mitochondrial function and loss of mitochondrial biogenesis factors (i.e., PGC-1α, NRF1, and TFAM). Transfection of the cells with miR-34a inhibitor (IB) halted HG-induced mitochondrial dysfunction and up-regulation of senescence-associated markers, whereas miR-34a mimic promoted cellular senescence and mitochondrial dysfunction. Moreover, HG lowered levels of the mitochondrial antioxidants TrxR2 and SOD2, an effect blunted by miR-34a IB, and promoted by miR-34a mimic. 3'-UTR (3'-untranslated region) reporter assay of both genes validated TrxR2 as a direct target of miR-34a, but not SOD2. Our results show that miR-34a is a key player of HG-induced SAPS in retinal endothelial cells via multiple pathways involved in mitochondrial function and biogenesis.
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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.