I am an assistant professor and principal investigator at Cincinnati Children’s, where my research focuses on understanding how transcription factors regulate biological processes and contribute to the diversity of life. I use the heart and cardiovascular system as a model to study these fundamental mechanisms, both because of their biomedical importance and because cardiac development is a remarkably complex and fascinating system. My lab is particularly interested in the transcription factor PITX2 and how its role in left-right developmental patterning may influence the later emergence of atrial fibrillation, the most common cardiac arrhythmia affecting millions of adults. Although human genetic studies consistently identify PITX2 as a major risk gene for atrial fibrillation, very little is known about how this transcription factor functions. By studying PITX2 directly, my work aims to uncover the molecular mechanisms that link developmental gene regulation to disease risk later in life.
My scientific interests grew out of my undergraduate training, where I became deeply engaged with evolutionary biology and evolutionary-developmental biology. During my doctoral studies, I was introduced to studying evolutionary principles in the context of congenital heart disease, which ultimately shaped the direction of my career. My PhD research explored evolutionarily conserved transcriptional patterning during lung formation and cardiac septation, work that naturally led me to continue studying the heart–lung interface during my postdoctoral training. There, I investigated pulmonary vein patterning and its relevance to atrial fibrillation, further solidifying my focus on developmental transcription factors and cardiovascular disease.
A key milestone in my transition to an independent lab was receiving a NIH K99/R00 Pathway to Independence Award. This work builds on my postdoctoral training and centers on defining how PITX2 regulates transcriptional repression in the context of atrial fibrillation, with the long-term goal of clarifying how early developmental programs shape disease susceptibility across the lifespan.
Although atrial fibrillation is typically considered a disease of aging, my research reflects a broader belief that understanding developmental patterning is essential for uncovering the roots of many diseases that manifest later in life. As a principal investigator, I lead the scientific vision of my laboratory while prioritizing mentorship and training for the next generation of scientists.
I am a Chicagoland native and earned my bachelor’s degree from the University of Notre Dame, my PhD from the University of Chicago, and completed postdoctoral training at Baylor College of Medicine. Outside the lab, I enjoy spending time with my growing family and our three dogs, and in my limited free time, I am an avid PC gamer.
BS: University of Notre Dame, Notre Dame, IN, 2011
PhD: University of Chicago, Chicago, IL, 2019
Postdoctoral Associated: Baylor College of Medicine, Houston, TX, 2025
Gene therapy CM-YAPon protects the mouse heart from myocardial infarction. Nature Cardiovascular Research. 2025; 4(12):1616-1626.
Single-nuclei transcriptomics reveals TBX5-dependent targets in a patient with Holt-Oram syndrome. Journal of Clinical Investigation. 2024; 135(2).
ETV2 primes hematoendothelial gene enhancers prior to hematoendothelial fate commitment. Cell reports. 2023; 42(6):112665.
Decoding the PITX2-controlled genetic network in atrial fibrillation. JCI Insight. 2022; 7(11).
Evolutionarily conserved Tbx5-Wnt2/2b pathway orchestrates cardiopulmonary development. Proceedings of the National Academy of Sciences of the United States of America. 2018; 115(45):E10615-E10624.
TEAD-independent mechanisms of YAP function in cardiomyocyte cell cycle reentry. Life Science Alliance. 2026; 9(4).
YAP-Induced Glycolysis Drives Fibroinflammation and Disrupts Fibroblast Fidelity. Circulation Research. 2025; 137(12):1443-1458.
PITX2 dosage-dependent changes in pacemaker cell state underlie sinus node dysfunction and atrial arrhythmias. Nature Communications. 2025; 16(1):11197.
SARS-CoV-2 NSP13 interacts with TEAD to suppress Hippo-YAP signaling. eLife. 2025; 13.
SARS-CoV-2 NSP13 interacts with TEAD to suppress Hippo-YAP signaling. eLife. 2025; 13.