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Cecilia Lo, PhD

Dr. Cecilia Lo is currently Distingished Professor of Developmental Biology, and F. Sargent Cheever Chair and Chair of the Department of Developmental Biology at the University of Pittsburgh School of Medicine.
 
Dr. Lo has had a longstanding interest in cardiovascular development and the genetic etiology of congenital heart disease.  Her laboratory conducted one of the largest mouse forward genetic screen to interrogate the genetic etiology of congenital heart disease.  

This led to the discovery of the central role of cilia biology and protein interactome network in driving the complex genetics of congenital heart disease. This screen also recovered the first model of hypoplastic left heart syndrome (HLHS), a congenital heart disease her screen demonstrated to have an obligate multigenic etiology.  

Her laboratory also has leveraged these findings in mice to pursue clinical translational studies. Recently she pioneered the use of patient induced pluripotent stem cells to model clinical outcome, demonstrating uncompensated oxidative stress from intrinsic mitochondrial defects as the likely cause for acute early heart failure in patients with HLHS.

LoPhotoC1_300x170_0.jpg

Cecilia Lo, PhD

Dr. Cecilia Lo is currently Distingished Professor of Developmental Biology, and F. Sargent Cheever Chair and Chair of the Department of Developmental Biology at the University of Pittsburgh School of Medicine.
 
Dr. Lo has had a longstanding interest in cardiovascular development and the genetic etiology of congenital heart disease.  Her laboratory conducted one of the largest mouse forward genetic screen to interrogate the genetic etiology of congenital heart disease.  

This led to the discovery of the central role of cilia biology and protein interactome network in driving the complex genetics of congenital heart disease. This screen also recovered the first model of hypoplastic left heart syndrome (HLHS), a congenital heart disease her screen demonstrated to have an obligate multigenic etiology.  

Her laboratory also has leveraged these findings in mice to pursue clinical translational studies. Recently she pioneered the use of patient induced pluripotent stem cells to model clinical outcome, demonstrating uncompensated oxidative stress from intrinsic mitochondrial defects as the likely cause for acute early heart failure in patients with HLHS.