Bio

​B.S. in Engineering Science, Pennsylvania State University, 2000Ph.D. in Bioengineering, University of California San Diego, 2005

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

Jeffrey Saucerman, Professor of Biomedical Engineering

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

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

Research Interests

  • Systems Biology
  • Cardiovascular Disease
  • Regenerative Medicine
  • Machine Learning and Data Science
  • Cellular and Molecular Engineering
  • Fibrosis
open Jeff Saucerman's Portrait

Jeffrey Saucerman, PhD, Professor of Biomedical Engineering, combines computational models and high-throughput experiments to discover molecular networks that control cardiac remodeling and regeneration.

In the News

Selected Publications

  • Matrix Biology 2020 ABS Computational model predicts paracrine and intracellular drivers of fibroblast phenotype after myocardial infarction
  • Front Physiol . 2019 ABS Multiscale Coupling of an Agent-Based Model of Tissue Fibrosis and a Logic-Based Model of Intracellular Signaling
  • Nat Rev Cardiol . 2019 ABS Mechanical regulation of gene expression in cardiac myocytes and fibroblasts
  • Circulation 2016 High-content phenotypic screen for compounds that induce proliferation of human iPSC-derived cardiomyocytes.
  • Biochim Biophys Acta. 2016 Knowledge gaps to understanding cardiac macrophage polarization following myocardial infarction.
  • J Mol Cell Cardiol. 2016 A computational model of cardiac fibroblast signaling predicts context-dependent drivers of myofibroblast differentiation.
  • J Mol Cell Cardiol. 2016 Computational modeling of cardiac fibroblasts and fibrosis.
  • Methods Mol Biol. 2015 Automated Microscopy of Cardiac Myocyte Hypertrophy: A Case Study on the Role of Intracellular α-Adrenergic Receptors.
  • Methods Mol Biol. 2014 Integrating fluorescent biosensor data using computational models.
  • Mol Pharmacol 2014 Modeling the effects of beta1-adrenergic receptor blockers and polymorphisms on cardiac myocyte Ca2+ handling.
  • J Biol Chem. 2014 A novel MitoTimer reporter gene for mitochondrial content, structure, stress and damage in vivo.
  • J Mol Cell Cardiol 2014 Phenotypic screen quantifying differential regulation of cardiac myocyte hypertrophy identifies CITED4 regulation of myocyte elongation.
  • J Gen Physiol. 2014 Mechanisms of cyclic AMP compartmentation revealed by computational models.
  • J Mol Cell Cardiol, 2013 PKA catalytic subunit compartmentation regulates contractile and hypertrophic responses to β-adrenergic stimulation.
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Courses Taught

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

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.