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Oxidative Stress Research

Researchers in the Center for Molecular Physiology closely study the impacts of reactive oxygen species (ROS), including free radicals and oxygen ions, to track the effect of their presence, and understand the role they play in cell signaling and other metabolic functions, with special emphasis on how these ROS participate in normal function of the kidneys. Additionally, the research team seeks to understand why and what happens when the level of ROS in the kidneys is too high, leading to a condition known as oxidative stress. Prolonged periods of oxidative stress are associated with a greater risk of hypertension and cardiovascular disease.

Oxidative Stress and Lipid Rafts
Peiying Yu, MD, tests the hypothesis that dopamine receptors in the kidney can regulate the activity of certain enzymes via lipid rafts. These lipid rafts, serve as a signaling platform to communicate necessary signals from and between a variety of cells, from the cell membranes itself. Dr. Yu has found that two mammalian dopamine D1-like receptors (D1R and D5R) regulate NADPH oxidase enzymes in lipid rafts of renal proximal tubule cells, which are cells that make up some of the primary tubes in the kidney. Quansheng Lu, MD, PhD, and Yu Yang, MD, PhD, study the role of antioxidants in the over-production of reactive oxygen species (ROS) in hypertension.

Oxidative Stress and Mitochondria
Hewang Li, MD, PhD, tests the hypothesis that the increased oxidative stress caused by the absence of a dopamine receptor known as D5R is due, in part, to increased production of ROS in mitochondria, a basic part of a cell that provides chemical energy and plays a role in proper signaling for regulation of proteins and enzymes. Increased mitochondrial production of ROS is important in understanding how oxidative stress may lead to essential hypertension. Mitochondria dysfunctions can lead to kidney disorders, which can interfere with movement of water and the excretion of salts (key functions of the kidney), and ultimately perhaps lead to hypertension. Preliminary studies suggest that the dopamine receptor known as D5R can decrease the mitochondria-ROS production in the kidney. This research seeks to understand how D5R regulates the mitochondrial ROS in the kidney, identify the signal pathways that are involved in this process, and examine mitochondria-generated ROS as a molecular, biochemical, and physiological biomarker of essential hypertension.

Faculty who study oxidative stress
 


   
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