My main focus of research is to characterize the mechanism of action of intracellular signaling pathways involved in the development of cardiac hypertrophy and its transition into heart failure, using different models such as the alcohol cardiomyopathy and volume-overload-induced cardiac hypertrophy. Of specific interest is the modulation of ion channels activities, and as such cardiac inotropy, by these pathways. Thus, I am actively working on the apoptotic and anti-apoptotic signaling related to the beneficial as well as the detrimental effects of chronic low versus high alcohol exposure, respectively, in the development of cardiac dysfunction and heart failure. My laboratory has found that alcohol activate the MAPKs and PI3K/Akt pathways, which have been shown to play a crucial role in the progression of cardiac contractile dysfunction and failure. Thus, my laboratory is on the forefront of studying the interactions between these kinases to modulate ionic channels activities and survival, especially in eccentric hypertrophy. In that regards, we have shown that not only PI3K/Akt activation is important for survival during cardiac hypertrophy and failure, but also acquires a major regulatory role on ion channels activities (IK1, IK and ICa,L). Such effects were found to be associated with cardiac dysfunctions during cardiomyopathy. On another note, my laboratory in collboartion with Boston University and Harvard university has undertaken an important endeavor in linking a genetic fingerprint to alcoholic cardiomyopathy in human. Due to the similarity in the volume-overload induced cardiac hypertrophy and obesity-related cardiac dysfunction, it is of great interest to elucidate the intricate relationship between apoptotic pathways and their causal relationship to changes in contractility during the setting of obesity-associated heart failure. In addition, I am starting to explore the role of cardiotropic peptides, such as CGRP and adipocytokines, in the precipitation of cardiac dysfunction and heart failure associated with obesity. My laboratory has already fostered collaborative relationships with other investigators in the field of cardiovascular diseases, gene therapy, gene sequencing and stem cell research which expanded our capabilities.