| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10953924 | Journal of Molecular and Cellular Cardiology | 2012 | 10 Pages |
Abstract
⺠Impaired cardiac leptin signaling exacerbates morbidity after myocardial infarction. ⺠Increased morbidity is linked to high rates of cardiac fatty acid oxidation. ⺠CNTF rescues cardiac survival kinase activity and glucose metabolism. ⺠CNTF is a potentially valuable therapy for myocardial infarction in obesity.
Keywords
TBARSMDAPDHObRAMPKCNTFPI3KAMP activated protein kinaseAdenosine TriphosphateATPSTATMyocardial infarctionFatty acidTotalciliary neurotrophic factorphosphorylated LeptinmalondialdehydeSignal transducer and activator of transcriptionMetabolismthiobarbituric acid-reactive substancespyruvate dehydrogenaseLeptin receptor
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Authors
William Witham, Keith Yester, Christopher P. O'Donnell, Kenneth R. McGaffin,