1. Calcium flux and endothelial dysfunction during acute lung injury: a STIMulating target for therapy
- Author
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Seeley, Eric J, Rosenberg, Paul, and Matthay, Michael A
- Subjects
Medical Physiology ,Biomedical and Clinical Sciences ,Acute Respiratory Distress Syndrome ,Lung ,Lung Cancer ,Physical Injury - Accidents and Adverse Effects ,Prevention ,Rare Diseases ,Cancer ,2.1 Biological and endogenous factors ,Aetiology ,Respiratory ,Acute Lung Injury ,Animals ,Calcium Channels ,Female ,Male ,Membrane Glycoproteins ,NADPH Oxidase 2 ,NADPH Oxidases ,Stromal Interaction Molecule 1 ,Medical and Health Sciences ,Immunology ,Biological sciences ,Biomedical and clinical sciences ,Health sciences - 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.
- Published
- 2013