NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart
By J. Kuroda, T. Ago, Shouji Matsushima, P. Zhai, M. Schneider, J. Sadoshima. Proceedings of the National Academy of Sciences of the United States of America, 2010
742 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/ceca6172135593bf239efdb9871e6fe767e52e12
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Citations in the corpus
- Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. (2014, background): “Nox4 is the only member of the family found to have a mitochondrial localization [in cultured mesangial cells (55), rat kidney cortex (55) and cardiac myocytes (251)].”
- Reperfusion injury and reactive oxygen species: The evolution of a concept (2015, background): “However, Nox4 has also been localized to the plasma membrane as well as ER and microsomal membranes [346,347].”
- Systems Genetics Approach Identifies Gene Pathways and Adamts2 as Drivers of Isoproterenol-Induced Cardiac Hypertrophy and Cardiomyopathy in Mice (2016, background): “The second, Nox4, which has a single output to Mfap5, has been previously established to be a key contributor to oxidative stress during pressure overload (Kuroda et al., 2010).”
- Crosstalk between mitochondria and NADPH oxidases (2011, background): “mitochondria of rat kidney cortex [98] and in the mitochondria of cardiac myocytes [99].”