Research areas ← All research areas

Overview

Background and objective: Ion channels control key functions of the CV system, from pacing the heart beat to triggering vascular smooth muscle contraction. Overall aim: Characterization of the ion channels and Ca2+ signals that participate in the normal functioning of the CV system, and how their dysfunction leads to disease. Projects and research teams: WP5 focus on ion channels and electrical remodelling (5.1) and Ca2+ signals (5.2). To carry out these projects basic teams with a clear translational vocation and clinical teams will be assembled, allowing research proposals with a balanced blend of CV clinicians, geneticists, electrophysiologists and molecular physiologist.

Project 1:

Electrical remodelling associated with atrial fibrillation and the hypertensive phenotype. Coordinator: J Tamargo.
Hypertension is the most prevalent risk factor for the development of atrial fibrillation (AF), the most common cardiac arrhythmia, which carries important complications (thromboembolisms). This project attempts to improve understanding of the ionic mechanisms that can be involved in the genesis and maintenance of AF in hypertensive patients. We will focus on two main aspects:

a) to determine the changes in expression and/or activity of human atrial Na+, Ca2+ and K+ (voltage dependent and inward rectifiers) channels produced by AF (electrical remodelling), with special attention to those involved in human atrial repolarization.

b) To determine the changes in expression and/or activity of smooth muscle ion channels in an animal model of essential hypertension.

Project 2:

Ion channels and Ca2+ signals in CVD. Coordinator: J Tarmargo.
Ca2+ signalling is of fundamental importance in the control of the vascular tone. Participating in the shaping of this signal are Ca2+ entry channels, intracellular Ca2+ stores and K+ channels that control the cell membrane potential.

Our project will tackle:

1. The role of K+ channels in smooth muscle proliferation, ischemic and neurodegenerative disease;
2. The molecular regulation voltage-gated and TRP channels;
3. The role of the endoplasmic reticulum ORMDL proteins in Ca2+ signals regulation.