A recent study co-authored by Northwestern Medicine scientists demonstrates a new molecular mechanism that may underlie left ventricular hypertrophy, a pattern of cardiac injury in which the heart’s main pumping chamber thickens and stiffens, eventually leading to heart failure.
The findings could lead to important applications for patients with chronic kidney disease, 75 percent of whom will develop left ventricular hypertrophy by the time they reach end-stage kidney disease.
“Left ventricular hypertrophy disproportionately affects the chronic kidney disease population due to a unique set of pathological factors,” said co-first author Dr. Ansel Amaral, a second-year resident in the Physician-Scientist Training Program and the department of medicine. “This study elucidated a molecular pathway that will provide a new target for pharmacological intervention in the near future.”
Working with scientists at the University of Miami, Dr. Amaral discovered that activating a cell surface protein called fibroblast growth factor receptor 4 (FGFR4) on heart muscle cells can induce left ventricular hypertrophy in animal models with and without kidney disease. The findings were published in Cell Metabolism.
“This suggests a new avenue for trying to prevent heart disease in settings where FGFR4 is excessively activated,” said Dr. Myles Wolf, director of the Center for Translational Metabolism and Health-Institute for Public Health and Medicine, who helped lead the research.
The scientists defined the cell-signaling pathway that mediates the hypertrophic growth of heart muscle cells in response to FGFR4 activation, and they showed that blocking FGFR4 with an antibody can help prevent the cardiac injury. Taken together, the study’s results suggest a cause of left ventricular hypertrophy that was not known before.
See journal article: http://www.cell.com/cell-metabolism/abstract/S1550-4131(15)00459-3