The proximal tubular α7 nicotinic acetylcholine receptor attenuates ischemic acute kidney injury through Akt/PKC signaling-mediated HO-1 induction

Abstract

Kidney injury: Nicotine and inflammation Nicotine may protect the kidney against ischemic reperfusion (IR) injury by reducing inflammation. IR injury is the tissue damage caused by a temporary block of blood flow leading to lack of oxygen and nutrient supply, followed by return of blood flow (reperfusion) resulting in excessive inflammation and oxidative stress. IR injury is the most common cause of acute kidney injury in hospitalized patients, sometimes leading to long-term kidney dysfunction. Sang Won Park and co-workers at the Gyeongsang National University School of Medicine, Jinju, South Korea investigated whether nicotinic receptor activation could reduce kidney injury in mice, using chemicals that stimulate or block the nicotine receptor. They found that stimulating the nicotine receptor decreased kidney inflammation and cell death through a kidney-specific molecular mechanism. These results may help treating kidney IR injury and long-term kidney dysfunction.