Our lab studies the diverse pathophysiological role of reactive oxygen species (ROS) such as superoxide radical, hydrogen peroxide, nitric oxide (NO·) and peroxynitrite. We were one of the first groups reported on development of mitochondrial oxidative stress and mitochondrial impairment under conditions of endothelial dysfunction and hypertension. Our lab has uncovered specific molecular mechanisms of mitochondrial ROS upregulation and their contribution in the development of hypertension by overexpression of mitochondrial superoxide dismutase (SOD2) and mitochondria targeted SOD mimetic antioxidants. Our team continues to develop a deeper understanding of the complex redox cell signaling pathways and oxidative stress in the pathogenesis of hypertension and other pathological conditions.
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Nashville, TN 37232
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MeSH terms are retrieved from PubMed records. Learn more.
Key: MeSH Term Keyword
Acetylcholine Animals Antigen-Presenting Cells Antineoplastic Agents, Phytogenic Antioxidants Aorta Brain Chemistry Calcium-Binding Proteins Caloric Restriction Cardiovascular System Catheterization Diabetes Mellitus Electron Spin Resonance Spectroscopy Endothelial Growth Factors Hemodynamics Hydrogen Hydrogen Peroxide Hypertension Hypoxia Infusion Pumps, Implantable Kinetics Lactic Acid Mitochondria Molecular Targeted Therapy Oxidative Stress Oxygen Consumption Reactive Nitrogen Species Respiratory Burst Reverse Transcriptase Inhibitors Rheology src-Family Kinases Stavudine Superoxide Dismutase Uric Acid Vasoconstriction Ventricular Fibrillation