Dr. Eric Small earned his B.S. degree in Cellular and Molecular Biology from the University of Michigan. He then completed a Ph.D. in the laboratory of Dr. Paul Krieg at the University of Texas at Austin, where he defined transcriptional mechanisms that regulate the early stages of heart development...
Dr. Eric Small earned his B.S. degree in Cellular and Molecular Biology from the University of Michigan. He then completed a Ph.D. in the laboratory of Dr. Paul Krieg at the University of Texas at Austin, where he defined transcriptional mechanisms that regulate the early stages of heart development. During subsequent post-doctoral training in Dr. Eric Olson's lab at UT Southwestern Medical Center at Dallas, he studied transcriptional and post-transcriptional mechanisms regulating gene expression in embryonic development and pathological cardiac remodeling. Dr. Small was recruited to the University of Rochester Medical Center in 2011. He is currently Associate Professor of Medicine at the Aab Cardiovascular Research Institute, with secondary appointments in Pharmacology and Physiology and Biomedical Engineering. Current research in the Small Lab focuses on defining mechanisms that control cardiac fibroblast plasticity and the development of pathological cardiac fibrosis.
Faculty Appointments
Professor
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Department of Medicine, Aab Cardiovascular Research Institute (SMD)
Professor
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Department of Biomedical Engineering (SMD) - Joint
Professor
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Department of Pharmacology and Physiology (SMD) - Joint
Credentials
Post-doctoral Training & Residency
UT Southwestern Medical Center at Dallas, Dallas, TX (Mentor: Eric N. Olson) 2005 - 2011
Hospital for Sick Children, Toronto, ON (Mentor: Benoit Bruneau) 2004 - 2005
Education
PhD | Univ Texas-Austin.Molecular Biology.2003
BS | University of Michigan.Cell and Molecular Biology.1995
Awards
Established Investigator Award.2023
Excellence in Postdoctoral Mentoring Award.2013
Scientist Development Grant.2010 - 2014
Ruth L. Kirschstein NRSA Post-Doctoral Fellowship.2004 - 2007
Best Poster Presentation Award.2002
Research
The overall goal of the Small lab is to better understand the mechanisms that control cell identity and lineage commitment by studying the transcriptional regulation and function of cardiac tissue-restricted genes. Our motivation is to decipher how disruption of cardiac gene expression programs in h...
The overall goal of the Small lab is to better understand the mechanisms that control cell identity and lineage commitment by studying the transcriptional regulation and function of cardiac tissue-restricted genes. Our motivation is to decipher how disruption of cardiac gene expression programs in heart disease contributes to cellular pathophysiology and the decline in cardiac function. There are two major themes of research within the lab that we study using mouse genetics, cell biology, advanced imaging, bioinformatic and biochemical approaches:
1. Cardiac fibroblast plasticity and the development of cardiac fibrosis. The transition to heart failure following cardiac insult is the result of irreversible cardiomyocyte loss and the development of cardiac fibrosis, which impedes contractility and can initiate lethal arrhythmias. Cardiac fibrosis arises from the aberrant and persistent stimulation of fibroblasts, the main source of extracellular matrix in the heart, in a pathological attempt to repair damaged tissue. We utilize gene expression profiling in animal models of heart disease and human heart failure patient samples to identify novel regulators of cardiac fibroblast accumulation and myofibroblast activation in health and disease. We also utilize high-throughput screening and pre-clinical animal studies to develop novel pharmacological and gene-targeting strategies to block or reverse cardiac scarring and the progression of heart failure.
2. Epicardium-derived progenitor cell mobilization. Epicardium-derived progenitor cells (EPDCs) can differentiate into cardiac fibroblasts and coronary blood vessels, and secrete signals that stimulate cardiac growth during embryonic development. We are striving to understand how EPDCs interpret developmental signals and differentiate into the appropriate cell type based upon their location within the heart. We have identified a mechanosensitive gene program that is essential for EPDC migration and subsequent differentiation into fibroblasts and perivascular cells. Ongoing studies are aimed at evaluating whether disruption of mechanosensitive transcriptional programs within the epicardium might contribute to cardiomyopathy. Our long-term goal is to harness the regenerative potential of the epicardium to improve cardiac repair.
Pérez-Hernández M, van Opbergen CJM, Bagwan N, Rasmus Vissing C, Marrón-Liñares GM, Zhang M, Torres Vega E, Sorrentino A, Drici L, Sulek K, Zhai R, Hansen FB, Hørby Christensen A, Boesgaard S, Gustafsson F, Rossing K, Small EM, Davies MJ, Rothenberg E, Sato P, Cerrone M, Jensen THL, Qvortrup K, Bundgaard H, Delmar M, Lundby A
Circulation.. 2022 September 13146 (11):851-867. Epub 08/12/2022.
Chi C, Leonard A, Knight WE, Beussman KM, Zhao Y, Cao Y, Londono P, Aune E, Trembley MA, Small EM, Jeong MY, Walker LA, Xu H, Sniadecki NJ, Taylor MR, Buttrick PM, Song K
Proceedings of the National Academy of Sciences of the United States of America.. 2019 January 8116 (2):556-565. Epub 12/24/2018.
Trembley MA, Quijada P, Agullo-Pascual E, Tylock KM, Colpan M, Dirkx RA, Myers JR, Mickelsen DM, de Mesy Bentley K, Rothenberg E, Moravec CS, Alexis JD, Gregorio CC, Dirksen RT, Delmar M, Small EM
Circulation.. 2018 October 23138 (17):1864-1878. Epub 1900 01 01.
Luna-Zurita L, Stirnimann CU, Glatt S, Kaynak BL, Thomas S, Baudin F, Samee MA, He D, Small EM, Mileikovsky M, Nagy A, Holloway AK, Pollard KS, Müller CW, Bruneau BG
Cell.. 2016 February 25164 (5):999-1014. Epub 02/11/2016.