Location
MR5 Room 2111 (inside the lab)
Lab
​MR5 Room 2213/2207
Box 800759 Health System
Charlottesville, VA 22908
Google Scholar ResearchGate PubMed Cardiac Systems Biology Group

About

Our lab combines computational modeling and high-throughput experiments to discover molecular networks and drugs that control cardiac remodeling and regeneration. Our experimental approaches include high-throughput microscopy and -omic profiling of primary and induced pluripotent stem cell (iPSC)-derived cardiomyocytes. Our computational approaches include large-scale regulatory network modeling and bioinformatic analysis of -omic data. Specific focus areas include:

  • cardiomyocyte hypertrophy and death
  • extra-cellular matrix remodeling by fibroblasts and macrophages
  • cardiomyocyte proliferation

Education

Ph.D. in Bioengineering, University of California San Diego, 2005

​B.S. in Engineering Science, Pennsylvania State University, 2000

We are mapping the complex networks that control heart function and failure

Jeffrey Saucerman Professor of Biomedical Engineering

Research Interests

Systems Biology
Cardiovascular Disease
Regenerative Medicine
Machine Learning and Data Science
Cellular and Molecular Engineering
Fibrosis

Selected Publications

Computational model predicts paracrine and intracellular drivers of fibroblast phenotype after myocardial infarction. Matrix Biology. 2020. A.C. Zeigler, A.R. Nelson, A.S. Chandrabhatla, O. Brazhkina, J.W. Holmes, J.J. Saucerman
Abstract
Multiscale Coupling of an Agent-Based Model of Tissue Fibrosis and a Logic-Based Model of Intracellular Signaling. Front Physiol. 2019. S.M. Rikard, T.L. Athey, A.R. Nelson, S.L.M. Christiansen, J. Lee, J.W. Holmes, S.M. Peirce, J.J. Saucerman
Abstract
Mechanical regulation of gene expression in cardiac myocytes and fibroblasts. Nat Rev Cardiol. 2019. J.J. Saucerman, P.M. Tan, K.S. Buchholz, A.D. McCulloch, J.H. Omens
Abstract
High-content phenotypic assay for proliferation of human iPSC-derived cardiomyocytes identifies L-type calcium channels as targets. Circulation. 2016. L.A. Woo, S. Tkachenko, M. Ding, A.T. Plowright, O. Engkvist, H. Andersson, L. Drowley, I. Barrett, M. Firth, P. Akerblad, M.J. Wolf, S. Bekiranov, D.L. Brautigan, Q. Wang, J.J. Saucerman
Abstract
Knowledge gaps to understanding cardiac macrophage polarization following myocardial infarction. Biochim Biophys Acta. 2016. M.L. Lindsey, J.J. Saucerman, K.Y. DeLeon-Pennell
Abstract
A computational model of cardiac fibroblast signaling predicts context-dependent drivers of myofibroblast differentiation. J Mol Cell Cardiol. 2016. A.C. Zeigler, W.J. Richardson, J.W. Holmes, J.J. Saucerman
Abstract
Computational modeling of cardiac fibroblasts and fibrosis. J Mol Cell Cardiol. 2016. A.C. Zeigler, W.J. Richardson, J.W. Holmes, J.J. Saucerman
Abstract
Automated microscopy of cardiac myocyte hypertrophy: a case study on the role of intracellular α-adrenergic receptors. Methods Mol Biol. 2015. K.A. Ryall, J.J. Saucerman
Abstract
Integrating fluorescent biosensor data using computational models. Methods Mol Biol. 2014. E.C. Greenwald, R.K. Polanowska-Grabowska, J.J. Saucerman
Abstract
Modeling the Effects of β1-Adrenergic Receptor Blockers and Polymorphisms on Cardiac Myocyte Ca2+ Handling. Mol Pharmacol. 2014.
R.K. Amanfu, J.J. Saucerman
Abstract
A novel MitoTimer reporter gene for mitochondrial content, structure, stress, and damage in vivo. J Biol Chem. 2014. R.C. Laker, P. Xu, K.A. Ryall, A. Sujkowski, B.M. Kenwood, K.H. Chain, M. Zhang, M.A. Royal, K.L. Hoehn, M. Driscoll, P.N. Adler, R.J. Wessells, J.J. Saucerman, Z. Yan
Abstract
Phenotypic screen quantifying differential regulation of cardiac myocyte hypertrophy identifies CITED4 regulation of myocyte elongation. J Mol Cell Cardiol. 2014. K.A. Ryall, V.J. Bezzerides, A. Rosenzweig, J.J. Saucerman
Abstract
Mechanisms of cyclic AMP compartmentation revealed by computational models. J Gen Physiol. 2014. J.J. Saucerman, E.C. Greenwald, R. Polanowska-Grabowska
Abstract
PKA catalytic subunit compartmentation regulates contractile and hypertrophic responses to β-adrenergic signaling. J Mol Cell Cardiol. 2013. J.H. Yang, R.K. Polanowska-Grabowska, J.S. Smith, C.W. Shields 4th, J.J. Saucerman
Abstract

Courses Taught

BME 2315 Computational Biomedical Engineering
BME 4550 Systems Bioengineering Modeling and Experimentation
BME 8315 Systems Bioengineering and Multi-Scale Models

Awards

Pinn Scholars Award 2018
NSF Faculty Early Career Development (CAREER) Award 2013
Dean's Excellence in Teaching Award 2012
Member, Academy of Distinguished Educators 2012
American Heart Association National Scientist Development Grant 2008
FEST Distinguished Young Investigator Grant 2007

Featured Grants & Projects

Cardiac hypertrophy Dozens of pathways are implicated in cardiac myocyte growth, but little is known about the quantitative contribution of these pathways to myocyte shape, reversibility, sarcomeric organization, or many other factors affecting the progression of heart failure. We are combining high-throughput microscopy, automated image processing, and large-scale network modeling to address these challenges.
Cardiac inflammation and extracellular matrix remodeling Cardiac macrophages and fibroblasts play important roles in inflammation and wound healing following cardiac injury. Yet systems and therapeutic approaches targeting these cells have been limited. We are collaborating with investigators at UVA and externally to reconstruct the molecular networks in fibroblasts and macrophages in the context of myocardial infarction.
Cardiac regeneration While cardiac regeneration was once thought to be limited to organisms such newts and zebrafish, recent studies have demonstrated that mammals also have some regenerative capacity. We are combining genomic and high-throughput microscopy experiments with computational models to map the molecular networks and identify compounds that stimulate cardiac myocyte proliferation.