A newly-discovered function for a receptor in heart muscle could change the way to design some cardiac drugs. The receptor, APJ, has been a target for drug makers because of its heart-healthy effects; for instance, it can help lower blood pressure.
But the new findings show that, if switched on in a different way, APJ can contribute to heart failure. What's important to heart failure is not if this receptor is "on" or "off" but the way it is activated. The discovery is described in a paper published today in Nature by Pilar Ruiz-Lozano, PhD, and colleagues, whose research was conducted at Stanford and at the Sanford-Burnham Medical Research Institute in La Jolla, Calif.
The new work helps scientists understand the connection between heart enlargement and heart failure. A strained heart gets bigger as it struggles to pump blood. Sometimes, the enlarged heart fails. The new research shows that APJ senses the stretching of an enlarged heart, and that the receptor is necessary for that stretch to be translated into a pathological heart-failure response. Mice lacking APJ were not vulnerable to heart failure from heart enlargement, the study showed.
From a Sanford-Burnham press release about the research:
“In other words, without APJ, ignorance is bliss—the heart doesn’t sense the danger and so it doesn’t activate the hypertrophic pathways that lead to heart failure,” Ruiz-Lozano said. “This tells us that, depending on how it’s done, activating APJ might make matters worse for heart disease patients.”
Previously: Heartening developments: Stanford expert discusses innovations in cardiac care and Failing at prescribing the best heart-failure treatments
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