Research ArticleAsthma

CaMKII Is Essential for the Proasthmatic Effects of Oxidation

See allHide authors and affiliations

Science Translational Medicine  24 Jul 2013:
Vol. 5, Issue 195, pp. 195ra97
DOI: 10.1126/scitranslmed.3006135

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

A Breath of Fresh Air for Asthma Patients

Reactive oxygen species (ROS) have a bad reputation, and rightly so. They’ve been implicated in contributing to a wide swath of diseases, including coronary heart disease, cancer, and asthma. Indeed, asthma is an increasing public health burden—affecting 8.5% of the population in the United States alone. Now Sanders et al. find that oxidative activation of the Ca2+/calmodulin-dependent protein kinase (ox-CaMKII) may respond to ROS in lung epithelium and contribute to asthma pathogenesis.

The authors observed that asthma patients have enhanced activation of ox-CaMKII in bronchial epithelium, which increases in response to inhaled antigen. Then they looked in two different mouse models of allergic asthma to examine the mechanistic connection. They found that blocking CaMKII either genetically or with a small-molecule inhibitor could alleviate ROS-mediated asthma progression. These data suggest that blocking CaMKII could be a new therapeutic strategy for asthma patients.

View Full Text

Stay Connected to Science Translational Medicine