title: Inhibition of the cardiomyocyte-specific troponin I-interacting kinase limits oxidative stress, injury, and adverse remodeling due to ischemic heart disease.
abstract: Ischemia–reperfusion injury is strongly associated with increased oxidative stress, mitochondrial dysfunction, and cell death. These processes are diminished in an animal model of ischemia–reperfusion by the genetic loss or pharmacological inhibition of troponin I–interacting kinase.
authors.affiliation: From the Department of Medicine, Division of Cardiology (D.M.A.) and Department of Molecular Genetics and Microbiology (D.A.M.), Duke University School of Medicine, Durham, NC.
authors.forename: Dennis M
authors.initials: DM
authors.lastname: Abraham
authors.forename: Douglas A
authors.initials: DA
authors.lastname: Marchuk
mesh_terms: D000818:Animals; D006801:Humans; D020930:MAP Kinase Kinase Kinases / Q000037:antagonists & inhibitors*; D017202:Myocardial Ischemia / Q000201:enzymology* / Q000503:physiopathology*; D018384:Oxidative Stress; D011494:Protein Kinases / Q000378:metabolism*; D020257:Ventricular Remodeling
chemical_list: D011494:Protein Kinases; D020930:MAP Kinase Kinase Kinases