Our research investigates transcriptional regulation mechanisms that link cardiac stress with altered myocardial fatty acid and glucose metabolism. Our long-term goal is to apply interventions that can improve cardiac function by modulating fatty acid oxidation and energy production.

We are interested in the role of Kruppel-like factors (KLFs)  and particularly, KLF5 and its role in the regulation of cardiac fatty acid oxidation during diabetes and ischemia/reperfusion. We also investigate the role of cardiomyocyte KLF5 in regulating systemic metabolism via an undiscovered cross-talk mechanism between the heart and the adipose tissue.

One of the projects in the lab focuses on the elucidation of the mechanisms that underlie sepsis-induced cardiac energy deprivation. The findings of our studies can be extrapolated to other types of cardiac dysfunction and propose novel therapies for the treatment of heart failure (HF).

Lab members

In addition to our longstanding research goals, we are interested in exploring the novel concept of metabolic dysfunction being involved in the pathogenesis of other diseases such as:
- Asthma: We are interested in identifying the metabolic profile of airway epithelial cells and role of fatty acid metabolism in mucin production.
- Spinal muscular atrophy: This is a neurodegenerative disease, which is the major cause for infant mortality and is caused by a gene mutation. The severe phenotype in humans and animal models is characterized by motor neuron loss and muscle atrophy, while cardiac dysfunction has also been reported. We are interested in investigating the metabolic profiles of the heart and neurons.