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Calcium flux and endothelial dysfunction during acute lung injury: a STIMulating target for therapy
Eric J. Seeley, … , Paul Rosenberg, Michael A. Matthay
Eric J. Seeley, … , Paul Rosenberg, Michael A. Matthay
Published February 22, 2013
Citation Information: J Clin Invest. 2013;123(3):1015-1018. https://doi.org/10.1172/JCI68093.
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Commentary

Calcium flux and endothelial dysfunction during acute lung injury: a STIMulating target for therapy

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Abstract

Bacterial pathogen-associated molecular pattern molecules (PAMPs) such as LPS activate the endothelium and can lead to lung injury, but the signaling pathways mediating endothelial injury remain incompletely understood. In a recent issue of the JCI, Gandhirajan et al. identify STIM1, an ER calcium sensor, as a key link between LPS-induced ROS, calcium oscillations, and endothelial cell (EC) dysfunction. In addition, they report that BTP2, an inhibitor of calcium channels, attenuates lung injury. This study identifies a novel endothelial signaling pathway that could be a future target for the treatment of lung injury.

Authors

Eric J. Seeley, Paul Rosenberg, Michael A. Matthay

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