| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5951944 | Cardiovascular Pathology | 2011 | 9 Pages |
Abstract
The results are consistent with the view that myocyte damage, fibrosis, and suppressed glycolytic flux represent maladaptive structural and metabolic remodeling that contribute to the development of failure in high pressure load-induced LVH in the mouse.
Keywords
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Authors
Michael E. Dunn, Thomas G. Manfredi, Arthur C. Cosmas, Frederick J. Vetter, Joshua N. King, Robert L. Rodgers,