Calmodulin kinase II inhibition protects against structural heart disease
By Rong-huai Zhang, M. Khoo, Yuejin Wu, Ying-bo Yang, Chad E. Grueter, G. Ni, E. Price, William H. Thiel, S. Guatimosim, Long‐Sheng Song and 9 more. Nature Medicine, 2005
619 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/aae7009d0ca87d0036246b8e0232ed7a1b552d67
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In Cardiology and Cardiovascular Medicine
In Molecular Biology
Citations in the corpus
- Regulation of cardiac hypertrophy by intracellular signalling pathways (2006, background): “The genetic inhibition of CaMKII reduced hypertrophy and improved cardiac function during infusion of isoproterenol, which indicated that CaMK is necessary and sufficient for the induction of cardiac hypertroph”
- A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidation. (2008, methodology): “, 2007) and AC3-I mice (Zhang et al., 2005) are protected from left ventricular dilation and dysfunction after myocardial infarction surgery, suggesting that ROS activation of CaMKII may be important in myocardial infarction.”
- Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress (2011, background): “, and genetic or pharmacologic CaMKII inhibition blocks ER-stress-induced apoptosis in a number of disease model”