2005- Postdoctoral training: University of Ottawa Heart Institue, Canada.
2010- Assistant Professor, College of Medicine, Alfaisal University, Saudi Arabia.
2020- Associate Professor, College of Medicine and Health Sciences, Khalifa University, United Arab Emirates.
The role of scaffold/membrane proteins in the decline of cardiac performance in hypertensive rats.
Hypertrophic obstructive cardiomyopathy is an insidious disease claiming thousands of lives on a daily basis due to the absence of an efficient management/therapy for hearts undergoing end-stage failure. The molecular mechanisms that control the pathological signaling of the diseased myocardium are not well understood. Hypertensive hearts remodel in response to pressure overload by increasing their muscle mass (hypertrophy) which, if kept untreated, progresses to dilatation of the cardiac chambers, and subsequently leads to failure and inevitable death. We are evaluating the genetic and protein profiling of the maladaptively remodeled hearts from an established animal model of essential hypertension, the Okamoto Spontaneously Hypertensive Rat (SHR). Data from this project is expected to further our understanding on the decline in contractile propensity of the hypertensive heart, and more precisely that of cardiac failure subsequent to dilation. It will serve as a translational platform for therapeutic strategies to attenuate the burden of maladaptive remodeling of the heart in humans, particularly within the United Arab Emirates population.
Molecular signature of the metabolomes in diabetic cardiomyopathy.
Diabetic cardiomyopathy is characterized by a decline in cardiac performance in diabetic subjects with absence of known cardiac risk factors (i.e. coronary artery disease, hypertension, valvular disease). There is paucity of information on the metabolic pathways implicated in this maladaptive remodeling of the diabetic heart. In addition, diabetes is often linked to vascular injuries namely coronary artery disease. The incomplete understanding of these clinical manifestations in diabetic hearts and in coronary arteries impose a critical barrier to progress towards a therapeutic strategy for these conditions. We are currently exploring the signalosomes that are acutely, or chronically, altered in diabetic hearts, with focus on the genetic profiling of diabetic patients. More precisely, we are investigating the dynamics of the calmodulin binding protein Striatin in diabetic cardiomyopathy and coronary artery disease. We are also examining the proteomic profiling and the metabolic signalosomes that promote these disorders to further our understanding on these conditions. Various techniques (in vitro, in vivo, and ex vivo) are employed to develop this project using animal models. Investigating these pathways in diabetic patients is a gold standard approach that we engage to translate our work bench-to-bedside and bedside-to-bench. The outcomes from this project may bypass the currently adopted therapeutic regimen to yield promising benefits for diabetic patients suffering from weakened myocardium.
Cardiac failure remains a major clinical and public health problem claiming millions of lives on a yearly basis. The rate of hospitalization and mortality of heart failure patients is not abating owing to paucity of information on the signaling pathways involved in the complexity of this pathology, and the near absence of an effective treatment for its derivative symptoms.
The Nader lab is broadly focused on mechanistic pathways and calcium homeostasis that are implicated in the onset and progression of cardiac failure. A special attention is given to metabolic disorders leading to cardiac dysfunction (i.e. Diabetes) and the role of membrane/scaffold proteins in these manifestations. We derive mechanistic insights into the membrane/scaffold proteins and protein phosphatase 2A (PP2A) in the maladaptive remodeling of the myocardium in diabetic and hypertensive animal models. We characterized a role for STRN in cardiomyocyte spontaneous contraction, and in the interaction between caveolin-3 and calmodulin in the heart. We are now deciphering the link between STRN and the adrenergic signaling in the myocardium, with focus on the derived adaptation of the heart in diabetes and hypertension conditions. We employ various in vivo, in vitro, and ex vivo methodologies to improve our understanding of the complexity of diabetes and hypertension induced cardiac failure syndrome.
We are also exploring the molecular signature of membrane/scaffold proteins and PP2A in vascular smooth muscle cells contraction, migration, and proliferation with special attention given to coronary artery disease (CAD). This is also inspected in the settings of diabetes and the resulting pathological remodeling of blood vessels. We combine clinical and empirical research data to translate our finding and advance our understanding of the etiology of CAD in diabetic patients.
We are well poised to challenge these cutting-edge goals and constantly offering training opportunities for those who are interested in embarking on these projects.
Trainees/Stduents who are interested in embarking on our ongoing projects and are seeking training opportunities in the Nader lab are invited to send their CV/request to the PI.