Molecular Cardiology

The major cardiovascular pathologies such as systemic hypertension, myocardial infarction and valvular heart disease induce injury to the heart and predispose to development of cardiac fibrosis and heart failure. The accumulation of extracellular matrix in the heart results in increased ventricular stiffness and disrupts the normal electrical cell-to-cell coupling and impulse conduction predisposing to arrhythmias and sudden cardiac death. This research aims at identifying signaling pathways regulating cardiac fibroblast function and development of cardiac fibrosis.

Small molecule kinase inhibitors (KIs) are a class of agents currently used for treatment of various cancers. Unfortunately, treatment of cancer patients with some of KIs is associated with cardiotoxicity and there is unmet need for methods to predict cardiotoxicity of them. One of the aims of our laboratory is to identify kinases and signaling pathway that are crucial for cardiac cell viability.

The standard of care for the prompt treatment of myocardial infarction and acute coronary syndromes are reperfusion therapies, including primary percutaneous coronary intervention and thrombolysis. Restoration of blood flow to ischemic myocardium limits infarct size and reduces mortality. Paradoxically, however, the return of blood flow can also result in additional cardiac damage and complications, referred to as reperfusion injury. Despite an improved understanding of the pathophysiology of this process and successful preclinical trials of multiple agents, most of the clinical trials to prevent or alleviate ischemia-reperfusion (I/R) injury have been disappointing, and therapies to reduce or prevent I/R injury do not exist. Our goal is to identify novel therapeutic approaches to target the development of I/R injury.