Sodium coupled neutral amino acid transporter SNAT2 counteracts cardiogenic pulmonary edema by driving alveolar fluid clearance.
This paper was published by Sarah Weidenfeld, C Chupin, DI Langner, T Zetoun et al @ American Journal of Physiology.
Acute respiratory distress syndrome (ARDS), the most frequent cause of death in intensive care, is characterized by an excessive inflammatory response, increased vascular permeability, edema formation, and impaired gas exchange. Recent studies have suggested deprivation of amino acids may aggravate lung injury while promoting apoptosis, ER stress, and autophagy. However, RCTs have failed to identify beneficial pharmaco‐nutritional interventions. This may point to a critical role of amino acid transporters in ARDS pathophysiology and its non‐human analogue acute lung injury (ALI). Sodium‐coupled neutral amino acid transporters (SNATs) mediate cellular uptake of amino acids along with Na+ and are known to be upregulated in response to amino acid starvation. They probed for the role of SNATs in a murine model of HCl‐ and LPS‐induced ALI and in a #pulmonary #epithelial cell culture system.
