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Farah Sheikh, PhD, FCVS, FAHA

Professor, UC San Diego School of Medicine

Dr. Farah Sheikh is a Professor in the Department of Medicine (Cardiovascular Medicine Division) at the University of California-San Diego in La Jolla, California, USA. She received her PhD in Cardiovascular Physiology from the University of Manitoba in 2001, which was focused on developing and testing multiple strategies to increase both cardiac muscle cell protection and regeneration through the regulation of the fibroblast growth factor-2 axis. For this work, she was awarded the 2001 E.L. Drewry Award (Faculty of Medicine) and 2001-2002 Distinguished PhD Dissertation Award in Health Sciences from the University of Manitoba. Her strong interests in understanding the genetic basis of human heart disease, led her to be recruited as a postdoctoral fellow at the University of California-San Diego (UCSD) in labs renown for exploiting genetic mouse models to understand human heart disease. She successfully obtained Canadian and US postdoctoral fellowship awards from the Canadian Institute of Health Research/Heart and Stroke Foundation and American Heart Association (AHA) to pursue her postdoctoral training. Her work exploited genetic mouse models to uncover novel central signaling effectors and components within the cytoskeleton and sarcomere that were critical towards the pathogenesis of dilated cardiomyopathy and heart failure progression. The impact of her studies led to several high impact publications and honors including the AHA Laverna Titus Young Investigator Awards, UCSD Schulman Award for Outstanding Cardiovascular Research, Badge of recognition by Faculty 1000 and being selected as a finalist for the prestigious AHA Louis N. and Arnold M. Katz Basic Research Prize. Based on her significant and creative contributions to research, she was recruited as faculty to the Department of Medicine at UCSD in 2009. Her specific research focus lies in identifying the pathways underlying biomechanical stress responses in the heart, which play a central role in the pathophysiology of cardiac disease and arrhythmias.