Dr. Mark Chandy

My research employs molecular biology to understand the pathophysiology of cardiovascular disease. Early in my career, I studied the mechanisms of chromatin dynamics, which have broad implications in the influence of the environment in conditions such as diabetes and smoking. I later helped characterize how transcription factors and microRNA direct cardiovascular differentiation and how perturbations of these mechanisms are implicated in cardiovascular disease. My interest in stem cell biology attracted me to Joseph Wu, MD, Ph.D. at Stanford, to learn more about human induced pluripotent stem cell (iPSC) disease modeling endothelial dysfunction.

Advances in next-generation sequencing, bioinformatics, and gene editing make it possible to decipher SNPs contributing to cardiovascular disease and disease-specific transcriptome profiles. More precise diagnostic biomarker-based tests could be developed with a deeper appreciation of an individual’s molecular signature. Additionally, personalized medicine could emerge from iPSC disease and advance precision medicine.

As a recently appointed Assistant Professor at the University of Western Ontario, I am now an independent physician-scientist conducting research using iPSC disease modeling that I developed at Stanford University. My research focuses on cardiovascular disease modeling to 1) investigate the effects of the environment on the vasculature, 2) discover biomarkers to risk stratify cardiovascular disease, and 3) discover druggable target genes for cardiovascular disease. The overarching goal of my research is to use iPSCs to understand mechanisms underlying the relationship between inherited factors and how environmental stress, such as diabetes, e-cigarettes, and marijuana, sensitize an individual to exacerbated cardiovascular disease. The discovery of these gene and environment interactions will facilitate the identification of high-risk individuals who could benefit from therapy that alters disease trajectory. In the future, iPSC disease modeling could guide the discovery of sm! all molec ule agonists or inhibitors that could be used as personalized medical therapy for cardiovascular disease.