title: Does endoplasmic reticulum stress mediate endothelin-1-induced renal inflammation?
abstract: Endothelin-1 (ET-1) is the most potent vasoconstrictor peptide known. It exerts its actions through two pharmacologically different receptors: ETA and ETB receptors. In the renal vasculature, there is a majority of ETB receptors in the efferent arteriole, whereas a greater amount of ETA receptors are located in the afferent arteriole. The nephron is rich in ETB receptors, especially in the thick ascending limb and collecting ducts, while containing a smaller amount of ETA receptors. High levels of circulating or renal ET-1 have been described in cardiovascular diseases such as hypertension or diabetes, diseases also associated to renal inflammation. Despite extensive evidence associating high levels of ET-1 to increased renal inflammation, the molecular mechanism(s) by which ET-1 leads to renal immune infiltration and/or immune activation remains unknown. In this minireview, we propose that the ET-1/ETA pathway mediates an increase in renal endoplasmic reticulum (ER) stress, initially a survival mechanism that if prolonged, leads to the eventual death of the cell via apoptosis.
authors.affiliation: Section of Experimental Medicine, Department of Medicine, Georgia Regents University, Augusta, GA 30912, USA.
authors.forename: Carmen
authors.initials: C
authors.lastname: De Miguel
authors.forename: Jennifer S
authors.initials: JS
authors.lastname: Pollock
mesh_terms: D000818:Animals; D059865:Endoplasmic Reticulum Stress / Q000502:physiology*; D019332:Endothelin-1 / Q000378:metabolism*; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007668:Kidney / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D017466:Receptors, Endothelin / Q000378:metabolism*; D014661:Vasoconstriction / Q000502:physiology
chemical_list: D019332:Endothelin-1; D017466:Receptors, Endothelin
keywords: endoplasmic reticulum stress; endothelin-1; renal inflammation