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Eric M. Small, Ph.D.

Contact Information

Phone Numbers

Administrative: (585) 276-7698

Office: (585) 276-7706

Fax: (585) 276-1530

Faculty Appointments

Biography

Professional Background

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.

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 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.

Credentials

Education

1995
BS | University of Michigan
Cell and Molecular Biology

2003
PhD | Univ Texas-Austin
Molecular Biology

Post-doctoral Training & Residency

0 - 2005
Hospital for Sick Children, Toronto, ON (Mentor: Benoit Bruneau)

0 - 2009
UT Southwestern Medical Center at Dallas, Dallas, TX (Mentor: Eric N. Olson)

Awards

2013
Excellence in Postdoctoral Mentoring Award

2010 - 2014
Scientist Development Grant
Sponsor: American Heart Association

2004 - 2007
Ruth L. Kirschstein NRSA Post-Doctoral Fellowship
Sponsor: National Institutes of Health

2002
Best Poster Presentation Award
Sponsor: Weinstein Cardiovascular Conference

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Publications

Journal Articles

4/2019
"Sacubitril/Valsartan Decreases Cardiac Fibrosis in Left Ventricle Pressure Overload by Restoring PKG Signaling in Cardiac Fibroblasts." Circulation. Heart failure.. 2019 Apr 0; 12(4):e005565.

2/13/2019
Quijada P, Misra A, Velasquez LS, Burke RM, Lighthouse JK, Mickelsen DM, Dirkx RA, Small EM. "Pre-existing fibroblasts of epicardial origin are the primary source of pathological fibrosis in cardiac ischemia and aging." Journal of molecular and cellular cardiology.. 2019 Feb 13; 129:92-104. Epub 2019 Feb 13.

1/31/2019
Hilt ZT, Pariser DN, Ture SK, Mohan A, Quijada P, Asante A, Cameron SJ, Sterling JA, Merkel AR, Johanson AL, Jenkins JL, Small EM, McGrath KE, Palis J, Elliott MR, Morrell CN. "Platelet-derived ?2M regulates monocyte inflammatory responses." JCI insight.. 2019 Jan 31; Epub 2019 Jan 31.

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