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Identified a mechanism responsible for the pathological response of the heart to sustained overload

Researchers from USA, Spain and Italy discovered a molecular mechanism responsible for the pathological response of the heart to intense and sustained overload. This mechanism is mediated by the APJ receptor, very similar to the angiotensin-receptor, and associated until now with a cardioprotective activity. The relevance of this finding lays in the fact that it was thought that the APJ function could only be beneficial for the heart. Some drugs are being designed aimed at increasing its activity.

The study was led by Dr. Pilar Ruiz-Lozano, a researcher at Stanford University, California, in collaboration with Dr. Perla Kaliman, who heads a team of the Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) in Barcelona. Both groups have been working together for more than 10 years in the study of cell signaling and development of cardiac pathology.

The role of Dr. Kaliman in Barcelona was centered in describing the intracellular signaling pathways of the receptor and confirming the data obtained previously in the USA: that the activation of APJ – which does indeed have a beneficial role for the heart in response to the hormone apelin – has very harmful effects when activated by continued mechanical stretch, which happens for example in response to hypertension. Under these conditions, the APJ receptor triggers reactions within the cardiocytes (heart cells) that result in hypertrophy and heart failure.

These results published by Nature mean an important warning for does drugs being designed to activate APJ indiscriminately, based on the hypothesis of its beneficial effects. Those drugs may be effective only with a dual action, reinforcing APJ beneficial activity while blocking its damaging effects.