Molecular Basis and Mechanisms of Cardiac Arrhythmias
Obesity is an important contributor to the increased risk of supraventricular arrhythmia incidence and mortality, suggesting that the obesity epidemic poses a significant public health problem, with over one-third of the world population being either overweight or obese. An important goal of my laboratory is to identify and validate novel pathways in the setting of metabolic disorders that will improve our knowledge of rational development of dietary and therapeutic interventions.
It is widely known that atrial fibrillation (AF), or rapid and irregular activation of the atrium, is the most common arrhythmia affecting both males and females. Therefore, our studies are designed to provide novel insights into the molecular basis of atrial electrical remodeling due to cardiac lipotoxicity with implications for supraventricular arrhythmia prevention. In this context, my laboratory has established a high-fat diet induced adult obese guinea pig model that will provide crucial insights into the ionic mechanisms that predispose obese patients to arrhythmias.
Another major area of my research laboratory is to develop tools and comprehensive approaches that will allow us to comprehensively assess the functional properties of K channels in heart. This would provide mechanistic insights into arrhythmias including atrial fibrillation (AF) and long QT syndrome (LQTS), which is underlain by congenital mutations in subunits (KCNQ1, KCNE1, hERG 1a/1b) that form the delayed rectifier K current (IK) . Recently, this research topic has contributed significantly to our understanding of the critical role of trafficking and gating mechanisms in the pathological decreases in the rapidly (IKr) and slowly (IKs) activating delayed rectifiers leading to prolongation of the action potential duration and predisposing to fatal arrhythmias such as Torsades de Pointes that lead to sudden cardiac death. Because LQTS can also be acquired in diabetes, we have recently developed a streptozotocin-induced diabetic adult guinea pig model and are currently characterizing the altered functional regulation of major cardiac ion channels (Ca, K, Na) involved in normal sinus rhythm.
- Guinea pig
- Langendorff perfused isolated heart
- Animal models of metabolic disorders (obesity, diabetes)
- Heterologous expression systems (HEK293, CHO cells)
- Molecular and Biochemistry approaches
- Adenoviral-associated gene transfer
- Optical and confocal imaging
- Flow cytometry
- Programmed electrical stimulation
Assistant Professor, MMRI
Email – , Phone – 315-624-7495
Dr. Aromolaran obtained a Master’s degree in Pharmacology from King’s College London and a PhD in Pharmacology from St Georges’ Hospital University of London. Dr. Aromolaran conducted his postdoctoral studies at Loyola University Chicago, where he obtained an American Heart Association postdoctoral fellowship to study the molecular and cellular mechanisms underlying the inositol 1,4,5-trisphosphate receptor (IP3R) mediated intracellular calcium regulation in cardiovascular diseases that involve ischemia. Dr. Aromolaran was appointed as instructor at Columbia University in 2010. During this time Dr. Aromolaran spearheaded a project using chemical tools for profiling and visualizing cardiac ion channels. This experience allowed him to successfully obtain an American Heart Association Scientist Development Grant and provided him with a unique opportunity to contribute to improving our knowledge of inherited and acquired arrhythmias. Dr. Aromolaran continued these studies as Research Scientist/Assistant Professor of Cell Biology at the VA Healthcare System NY Harbor/SUNY Downstate Brooklyn, where he obtained an NHLBI R01 that will allow him to further investigate mechanisms that underlie arrhythmias acquired in metabolic disorders. This knowledge and interest in arrhythmias underlain by pathological conditions has led Dr. Aromolaran to the Masonic Medical Research Institute, where the goal of his Cardiac Electrophysiology and Metabolism research group is to identify and validate novel metabolic disorder (obesity, diabetes, lipotoxicity) signaling pathways that may modulate cardiac ion channel function and reveal molecular insights that will facilitate development of novel and targeted dietary and/or therapeutic interventions. Dr. Aromolaran’s research is funded by the AHA and NIH, and he has served on review boards, institutional committees, and AHA and NIH study sections. Dr. Aromolaran served as faculty and co-director of the NHLBI-funded program to increase diversity in cardiovascular research and is also actively involved in training and mentoring students, MDs and PhDs.
- American Heart Association
- Biophysical Society
- Heart Rhythm Society
- Assistant Professor of Cardiovascular Medicine, Masonic Medical Research Institute
- Ph.D., Pharmacology St George’s Hospital University of London
- M.Sc., Pharmacology King’s College London
- Graduate Certificate in Regulatory Affairs; Massachusetts College of Pharmacy and Health Sciences
Ongoing Research Support
- 1R01HL147044-01, A. Aromolaran (PI) 05/1/2019-02/23/2023.
Completed Research Support
- AHA Scientist Development Grant, 13SDG16850065, A. Aromolaran (PI)- 2013-2018
- AHA postdoc fellowship 0325564Z, A. Aromolaran (PI), 2003 - 2005
- Jenny Do
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