Authors: Allen Titus, Yasuki Nakada, Wataru Mizushima, Yanfei Yang, Peiyong Zhai, Shinichi Oka, Toshihide Kashihara, Nadezhda Fefelova, Tong Liu, Hong Li, Lai-Hua Xie, Junichi Sadoshima
Published: 2024-10-09
DOI: 10.1161/res.135.suppl_1.tu128
Source: Full article
Introduction: Elevated oxidative stress linked with heart failure is a major cause for the downregulation of sarcoplasmic/endoplasmic reticulum (SR/ER) Ca2+ ATPase 2a (SERCA2a). NADPH oxidase (NOX) complexes are a key source of reactive oxygen species (ROS) in cardiomyocytes. p22phox, a transmembrane partner of NOX1-4, plays an essential role in mediating ROS production in multiple NOX complexes. We investigated the role of p22phox in oxidative stress and SERCA2a levels during pressure overload (PO).