American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Mar 2017
Experimental Lung Injury Reduces KLF2 to Increase Endothelial Permeability via Regulation of RAPGEF3-Rac1 Signaling.
Acute respiratory distress syndrome (ARDS) is caused by widespread endothelial barrier disruption and uncontrolled cytokine storm. Genome-wide association studies (GWAS) have linked multiple genes to ARDS. Although mechanosensitive transcription factor Krüppel-like factor 2 (KLF2) is a major regulator of endothelial function, its role in regulating pulmonary vascular integrity in lung injury and ARDS-associated GWAS genes remains poorly understood. ⋯ Disruption of endothelial KLF2 results in dysregulation of lung microvascular homeostasis and contributes to lung pathology in ARDS.