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Updated: Apr 17, 2026

Analysis of Oxidative Stress in Zebrafish Embryos
Published on: July 7, 2014
Oxidative stress, NADPH oxidases, and arteries
Qi-An Sun, Marschall S Runge1, Nageswara R Madamanchi
1Marschall S. Runge, MD PhD, Department of Medicine, 125 MacNider Hall, University of North Carolina, Chapel Hill, NC 27599-7005, USA,
Insights
Cardiovascular diseases like heart attack and stroke are major health threats. Targeting nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) may help prevent these conditions by reducing oxidative stress.
Area of Science:
- Cardiovascular Research
- Oxidative Stress Biology
- Molecular Medicine
Background:
- Atherosclerosis, myocardial infarction, and stroke are leading causes of death globally.
- Rising obesity and diabetes mellitus exacerbate the public health impact of cardiovascular diseases (CVD).
- Oxidative stress is a key mechanistic factor linking various CVD risk factors.
Purpose of the Study:
- To investigate the role of oxidative stress in cardiovascular diseases.
- To explore the function of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) in vascular cells.
- To assess the potential of targeting NADPH oxidase for CVD prevention.
Main Methods:
- Utilizing animal models to study the interplay between oxidative stress and CVD.
- Analyzing the expression and activity of NADPH oxidase components in vascular tissues.
- Evaluating the impact of modulating NADPH oxidase on atherosclerosis and hypertension.
Main Results:
- NADPH oxidases are critically important in the development of atherosclerosis and hypertension in animal models.
- Vascular cells generate reactive oxygen species primarily through NADPH oxidase enzymes.
- Emerging evidence highlights the significance of NADPH oxidases in cardiovascular pathology.
Conclusions:
- NADPH oxidases play a crucial role in mediating vascular oxidative stress.
- Tissue-specific expression of NADPH oxidase components offers potential therapeutic targets.
- Targeting vascular oxidative stress via NADPH oxidase inhibition may be a viable strategy for CVD prevention.
Abstract:
Atherosclerosis and its major complications - myocardial infarction and stroke - remain major causes of death and disability in the United States and world-wide. Indeed, with dramatic increases in obesity and diabetes mellitus, the prevalence and public health impact of cardiovascular diseases (CVD) will likely remain high. Major advances have been made in development of new therapies to reduce the incidence of atherosclerosis and CVD, in particular for treatment of hypercholesterolemia and hypertension. Oxidative stress is the common mechanistic link for many CVD risk factors. However, only recently have the tools existed to study the interface between oxidative stress and CVD in animal models. The most important source of reactive oxygen species (and hence oxidative stress) in vascular cells are the multiple forms of enzymes nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase). Recently published and emerging studies now clearly establish that: 1) NADPH oxidases are of critical importance in atherosclerosis and hypertension in animal models; 2) given the tissue-specific expression of key components of NADPH oxidase, it may be possible to target vascular oxidative stress for prevention of CVD.
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