Poster Title (Current Submission)

Antioxidants, Heart Disease, and Nox4 in Between

Major(s)

Integrative Physiology

Mentor Name

Francis Miller

Other Mentor Department

Internal Medicine

Presentation Date

3-25-2010

Abstract

The Center for Disease Control reports coronary artery disease (CAD) as the leading cause of heart attacks in the United States. Recently there has been talk of oxidants, antioxidants, and lipids, but it is unclear exactly how all of these function or dysfunction when it comes to CAD. With the knowledge that in clinical trials antioxidants do not prevent CAD, our study aims to better understand how oxidants and antioxidants function in the inflammatory responses of smooth muscle cells, ultimately leading to plaque formation. Here we show that the oxidant producing protein, NADPH Oxidase 4 (Nox4) regulates the concentration of key antioxidants of the cell, and maintains cell survival against oxidative insults. These findings implicate Nox4 as a survival signal during conditions a cell might otherwise choose death. This increased survival capacity could ultimately lead to the accumulation of cells in a lesion on the vessel wall that forms CAD.

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Mar 25th, 12:00 AM

Antioxidants, Heart Disease, and Nox4 in Between

The Center for Disease Control reports coronary artery disease (CAD) as the leading cause of heart attacks in the United States. Recently there has been talk of oxidants, antioxidants, and lipids, but it is unclear exactly how all of these function or dysfunction when it comes to CAD. With the knowledge that in clinical trials antioxidants do not prevent CAD, our study aims to better understand how oxidants and antioxidants function in the inflammatory responses of smooth muscle cells, ultimately leading to plaque formation. Here we show that the oxidant producing protein, NADPH Oxidase 4 (Nox4) regulates the concentration of key antioxidants of the cell, and maintains cell survival against oxidative insults. These findings implicate Nox4 as a survival signal during conditions a cell might otherwise choose death. This increased survival capacity could ultimately lead to the accumulation of cells in a lesion on the vessel wall that forms CAD.