A new study by University of Hawaiʻi researchers identifies a molecular pathway that may help reduce the damaging effects of an enlarged heart caused by hypertension or a heart attack.
The study by researchers in UH Mānoa’s John A. Burns School of Medicine and UH Hilo’s College of Pharmacy demonstrates for the first time that stretching of cardiac cells in cardiac hypertrophy promotes secretion of a protein that helps protect cardiac function and keep cardiac cells alive.
Vascular Endothelial Growth Factor, or VEGF, normally creates new blood vessels during embryonic development and promotes vessel development following injury or lack of oxygen. In a study using rats, Assistant Professor of Molecular Biology Michelle Matter and her colleagues found that when enlargement of the heart stretches cardiac cells, they release VEGF.
“We have found that stretch of adult cardiac cells promotes release of VEGF through activation of the NFkB signaling pathway,” Matter said. Blocking NFkB activation abrogates VEGF secretion induced by cyclic mechanical stretch in these cells.
“Targeting this molecular pathway may alleviate the pathological effects of hypertrophy and increase survival of patients who have had a heart attack or suffer hypertension,” Matter said.
Heart disease in Hawaiʻi
More than 3,100 people in Hawaiʻi die of cardiovascular disease each year, according to The Burden of Heart Disease in Hawaiʻi, a report to the state Department of Health.
As many as 70 percent of the adults in Hawaiʻi have at least one risk factor for cardiovascular disease, including diabetes, hypertension and obesity, and Big Island residents, Native Hawaiians, Filipinos and the poor have higher risks for cardiovascular disease, according the DOH report.
About the study
Study co-authors are Anna Leychenko and Mayumi Jijiwa of the UH Mānoa Department of Cell and Molecular Biology and Eugene Konorev of the UH Hilo College of Pharmacy.
The research was funded by the National Institutes of Health’s National Center for Research Resources and the results published online in the journal PLoS ONE during December 2011.