Genetic ablation of Nrf2 enhances susceptibility to cigarette smoke–induced emphysema in mice
Emphysema is a major manifestation of chronic obstructive lung disease, which affects more than 16 million Americans and is the fourth highest cause of death in the United States. This disease is primarily cigarette smoke induced, but oxidative stress, a harmful condition that occurs when there is an excess of free radicals, has recently been alleged to play an important role in lung susceptibility to cigarette smoke-induced damage.
To investigate the impact of oxidative stress on emphysema development, Shyam Biswal and colleagues, from Johns Hopkins University, disrupted in mice the nuclear factor, erythroid-derived 2, like 2 (Nrf2) gene, which makes a protein that regulates genes involved in protecting the body from free radical damage. The authors found that cigarette smoke-induced emphysema was of earlier onset and more widespread in the Nrf2–/– mice than in their wild-type littermates. The Nrf2–/– mice also had a greater number of alveolar cells that underwent programmed cell death, and had more prominent bronchoalveolar inflammation.
Laurie Goodman | EurekAlert!
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