A multidisciplinary team of researchers, led by Henrique Girão, from the Faculty of Medicine of the University of Coimbra (FMUC), identified a protein that can compromise communication between the cells responsible for the propagation of the heart’s contraction signal, contributing to the emergence of diseases heart attacks.
In particular, in this study, which included the participation of the Coimbra Hospital and University Center (CHUC) and the Faculty of Medicine of the University of Porto (FMUP), it was discovered that “the EHD1 protein is crucial to regulate the distribution and location of a channel – called gap junction – which is essential for the rapid propagation of the electrical signal through the heart muscle, and which is at the base of the synchronized heartbeat ”, states Henrique Girão.
In order to better understand the relevance of this research, the results of which are already published in the renowned scientific journal Circulation Research, the FMUC researcher explains that “in a healthy heart, to ensure a competent conduction of the “sign of contraction”, these channels [gap junctions] they are located in certain areas of the surface of the heart muscle cells, called intercalated discs.
For this reason, many heart diseases are associated with an abnormal distribution of gap junctions in the cells of the heart, with their exit from the intercalated discs, which has a negative impact on the propagation efficiency of the electric wave and, consequently, on the force of contraction“.
In these cases, he clarifies, “the heartbeat is less vigorous, making less blood to be ejected (pumped) in each contraction. In this study we see how, in sick hearts, the gap junctions are redistributed in cardiac cells. Our results show that EHD1 participates in the process of removing gap junctions from intercalated discs, leading, then, to their accumulation in other areas of the cell, where the role of these channels in the rapid propagation of the electrical signal is compromised“.
The results of this study, which was funded by the Foundation for Science and Technology (FCT) and lasted for four years, clarify the mechanisms through which this redistribution of gap junctions occurs in the sick heart, enabling “the identification of new targets treatments that allow, in the future, the development of more effective approaches to fight cardiovascular diseases, particularly innovative strategies that prevent the EHD1 protein from participating in the removal of gap junctions of the interim discs, thus guaranteeing an efficient heartbeat”, concludes Henrique Girão.