Abstract
AbstractDietary high salt (HS) is a major risk factor for cardio-vascular and chronic inflammatory diseases. Sodium can increase postprandially but can also accumulate in diverse tissues. Immune cells, such as macrophages, sense this salty environment and adapt accordingly, shifting towards a more pro-inflammatory state. Mechanistically, HS inhibits complex II of the electron transport chain and thereby reduces mitochondrial function. In two independent clinical studies, an HS-diet transiently impaired human monocytic mitochondrial function.
Publisher
Springer Science and Business Media LLC
Subject
Molecular Biology,Biotechnology