Inhibition of the cardiomyocyte-specific troponin I-interacting kinase limits oxidative stress, injury, and adverse remodeling due to ischemic heart disease.

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Abraham, DM; Marchuk, DA

Published Date

  • March 14, 2014

Published In

Volume / Issue

  • 114 / 6

Start / End Page

  • 938 - 940

PubMed ID

  • 24625723

Pubmed Central ID

  • 24625723

Electronic International Standard Serial Number (EISSN)

  • 1524-4571

Digital Object Identifier (DOI)

  • 10.1161/CIRCRESAHA.113.303238

Language

  • eng

Conference Location

  • United States