ArticleDiabetes2013
Cell-based screening identifies paroxetine as an inhibitor of diabetic endothelial dysfunction.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- Effectiveness of Paroxetine Versus Non-Paroxetine Selective Serotonin Reuptake Inhibitors on Mortality and Heart Failure Following Myocardial Infarction: An Active Comparator Population-Based Cohort Study.Pharmacoepidemiology and drug safety · 2025Article
- The selective serotonin reuptake inhibitor paroxetine improves right ventricular systolic function in experimental pulmonary hypertension.Journal of molecular and cellular cardiology plus · 2024Article
- Glucose dysregulation in antipsychotic-naive first-episode psychosis: in silico exploration of gene expression signatures.Translational psychiatry · 2024Article
- Modeling diabetic endothelial dysfunction with patient-specific induced pluripotent stem cells.Bioengineering & translational medicine · 2023Article
- Different Effects of SSRIs, Bupropion, and Trazodone on Mitochondrial Functions and Monoamine Oxidase Isoform Activity.Antioxidants (Basel, Switzerland) · 2023Article
- Systemic DNA and RNA damage from oxidation after serotonergic treatment of unipolar depression.Translational psychiatry · 2022Article
- A case study of a patient-centered reverse translational systems-based approach to understand adverse event profiles in drug development.Clinical and translational science · 2022Article
- Mitochondrial dysfunction in vascular endothelial cells and its role in atherosclerosis.Frontiers in physiology · 2022Review
- Off-Target Effects of Antidepressants on Vascular Function and Structure.Biomedicines · 2021Review
- Redox metabolism modulation as a mechanism in SSRI toxicity and pharmacological effects.Archives of toxicology · 2020Review
- The effect of fluoxetine on astrocyte autophagy flux and injured mitochondria clearance in a mouse model of depression.Cell death & disease · 2019Article
- Current state and outlook for drug repositioning anticipated in the field of ovarian cancer.Journal of gynecologic oncology · 2019Review
- Development of a stretch-induced neurotrauma model for medium-throughput screening in vitro: identification of rifampicin as a neuroprotectant.British journal of pharmacology · 2018Article
- In the View of Endothelial Microparticles: Novel Perspectives for Diagnostic and Pharmacological Management of Cardiovascular Risk during Diabetes Distress.Journal of diabetes research · 2018Review
- Impact of Muscarinic MCNS drugs · 2017Article
- The novel mitochondria-targeted hydrogen sulfide (HPharmacological research · 2016Article
- Hydrogen Sulfide Selectively Inhibits γ-Secretase Activity and Decreases Mitochondrial Aβ Production in Neurons from APP/PS1 Transgenic Mice.Neurochemical research · 2016Article
- Glucocorticoids Suppress Mitochondrial Oxidant Production via Upregulation of Uncoupling Protein 2 in Hyperglycemic Endothelial Cells.PloS one · 2016Article
- Salvage of nicotinamide adenine dinucleotide plays a critical role in the bioenergetic recovery of post-hypoxic cardiomyocytes.British journal of pharmacology · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have conducted a phenotypic screening in endothelial cells exposed to elevated extracellular glucose (an in vitro model of hyperglycemia) to identify compounds that prevent hyperglycemia-induced reactive oxygen species (ROS) formation without adversely affecting cell viability. From a focused library of >6,000 clinically used drug-like and pharmacologically active compounds, several classes of active compounds emerged, with a confirmed hit rate of <0.5%. Follow-up studies focused on paroxetine, a clinically used antidepressant compound that has not been previously implicated in the context of hyperglycemia or diabetes. Paroxetine reduced hyperglycemia-induced mitochondrial ROS formation, mitochondrial protein oxidation, and mitochondrial and nuclear DNA damage, without interfering with mitochondrial electron transport or cellular bioenergetics. The ability of paroxetine to improve hyperglycemic endothelial cell injury was unique among serotonin reuptake blockers and can be attributed to its antioxidant effect, which primarily resides within its sesamol moiety. Paroxetine maintained the ability of vascular rings to respond to the endothelium-dependent relaxant acetylcholine, both during in vitro hyperglycemia and ex vivo, in a rat model of streptozotocin-induced diabetes. Thus, the current work identifies a novel pharmacological action of paroxetine as a protector of endothelial cells against hyperglycemic injury and raises the potential of repurposing of this drug for the experimental therapy of diabetic cardiovascular complications.
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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.