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Coenzyme Q10 Alleviates Chronic Nucleoside Reverse Transcriptase Inhibitor-Induced Premature Endothelial Senescence.
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- Cardiovascular Toxicology, 2019, v. 19, n. 6, p. 500, doi. 10.1007/s12012-019-09520-1
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- Article
Role of COX-2 in the Bioactivation of Methylenedianiline and in Its Proliferative Effects in Vascular Smooth Muscle Cells.
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- Cardiovascular Toxicology, 2011, v. 11, n. 4, p. 316, doi. 10.1007/s12012-011-9123-1
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- Article
Synergistic effect of resveratrol and quercetin released from drug-eluting polymer coatings for endovascular devices.
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- Journal of Biomedical Materials Research, Part B: Applied Biomaterials, 2011, v. 99B, n. 2, p. 266, doi. 10.1002/jbm.b.31894
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- Article
Radical-Containing Ultrafine Particulate Matter Initiates Epithelial-to-Mesenchymal Transitions in Airway Epithelial Cells.
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- American Journal of Respiratory Cell & Molecular Biology, 2013, v. 48, n. 2, p. 188, doi. 10.1165/rcmb.2012-0052OC
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- Article
Oral delivery of xenon for cardiovascular protection.
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- Scientific Reports, 2019, v. 9, n. 1, p. N.PAG, doi. 10.1038/s41598-019-50515-3
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- Article
Stress‐induced premature senescence as a mechanism of nucleoside reverse transcriptase inhibitor‐induced endothelial dysfunction (547.18).
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- FASEB Journal, 2014, v. 28, p. N.PAG, doi. 10.1096/fasebj.28.1_supplement.547.18
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- Article
Particulate matter containing environmentally persistent free radicals induces AhR-dependent cytokine and reactive oxygen species production in human bronchial epithelial cells.
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- PLoS ONE, 2018, v. 13, n. 10, p. 1, doi. 10.1371/journal.pone.0205412
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- Article
4,40-Methylenedianiline Alters Serotonergic Transport in a Novel, Sex-Specific Model of Pulmonary Arterial Hypertension in Rats.
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- Toxicological Sciences, 2015, v. 147, n. 1, p. 235, doi. 10.1093/toxsci/kfv126
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- Article
Nucleoside Reverse Transcriptase Inhibitors Induce a Mitophagy-Associated Endothelial Cytotoxicity That Is Reversed by Coenzyme Q10 Cotreatment.
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- Toxicological Sciences, 2013, v. 134, n. 2, p. 323, doi. 10.1093/toxsci/kft105
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- Article
Antiretrovirals Induce Endothelial Dysfunction via an Oxidant-Dependent Pathway and Promote Neointimal Hyperplasia.
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- Toxicological Sciences, 2010, v. 117, n. 2, p. 524, doi. 10.1093/toxsci/kfq213
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- Article