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Reversing 'hibernating' heart muscle focus of UB researchers

Heart researchers at the University at Buffalo have received a $2.5 million five-year grant to develop new strategies to reverse a heart dysfunction called "hibernating myocardium" that can cause disabling heart failure and sudden death.

Hibernating myocardium is a condition in which myocytes (cells in the heart's muscular tissue) shut down, but remain viable in areas that receive reduced blood flow over an extended period of time due to narrowed arteries. This creates areas of the heart that contract poorly.

The new grant from the National Heart Lung and Blood Institute builds on pioneering work of scientists in UB's Center for Research in Cardiovascular Medicine who developed a novel pig model with hibernating myocardium.

Previous research has shown that, while restoring blood flow to these "hibernating" regions improves function and a patient's prognosis, cells in the left ventricle (the heart's main pumping chamber) often remain chronically dysfunctional and do not return to normal. The reasons for this remain unclear, researchers say, but in most circumstances do not appear to be caused by replacement with scar tissue.

The new grant will allow researchers to determine if the metabolic changes that myocytes undergo in order to remain viable during hibernation limit their long-term ability to recover fully after revascularization.

John M. Canty, M.D., Albert and Elizabeth Rekate Chair in Cardiovascular Disease in the UB School of Medicine and Biomedical Sciences and chief of the Division of Cardiovascular Medicine, is principal investigator on the grant. Canty is a head of the Cardiovascular Disease Group of the New York State Center of Excellence in Bioinformatics and Life Sciences at UB.

The researchers will undertake concurrent physiological, proteomic and mitochondrial functional studies in the swine model that will be translatable to humans. Proteomic profiling will identify candidate mitochondrial
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Source:University at Buffalo


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