학술논문

Calcium flux and endothelial dysfunction during acute lung injury: a STIMulating target for therapy
Document Type
article
Source
Journal of Clinical Investigation. 123(3)
Subject
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
Language
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.