title: Calcium flux and endothelial dysfunction during acute lung injury: a STIMulating target for therapy.
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: Cardiovascular Research Institute and Department of Medicine, UCSF, San Francisco, California 94143, USA.
authors: Eric J
authors: EJ
authors: Seeley
authors: Paul
authors: P
authors: Rosenberg
authors: Michael A
authors: MA
authors: Matthay
mesh_terms: D055371:Acute Lung Injury / Q000517:prevention & control*; D000818:Animals; D015220:Calcium Channels; D005260:Female; D008297:Male; D008562:Membrane Glycoproteins / Q000037:antagonists & inhibitors*; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases / Q000037:antagonists & inhibitors*; D000071737:Stromal Interaction Molecule 1
chemical_list: D015220:Calcium Channels; D008562:Membrane Glycoproteins; C100757:Stim1 protein, mouse; D000071737:Stromal Interaction Molecule 1; C488842:Cybb protein, mouse; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases