Downregulation of endothelin A receptor (ETaR) ameliorates renal ischemia reperfusion injury by increasing nitric oxide production

Abstract

ETaR siRNA treatment inhibited inflammatory response and improved renal function after renal IRI. The underlying mechanisms of ETaR siRNA treatment may be through increasing eNOS activity through PI3K/Akt signaling, which subsequently increased NO production. The increased NO reduces the expression of ET-1 by inhibiting transcription of ET-1-associated genes via the sGC/PKG signaling pathway.