Artistoo, a library to build, share, and explore simulations of cells and tissues in the web browser

  1. Inge M N Wortel  Is a corresponding author
  2. Johannes Textor  Is a corresponding author
  1. Radboud University, Netherlands
  2. Radboud Institute for Molecular Life Sciences, Netherlands


The Cellular Potts Model (CPM) is a powerful in silico method for simulating biological processes at tissue scale. Their inherently graphical nature makes CPMs very accessible in theory, but in practice, they are mostly implemented in specialised frameworks users need to master before they can run simulations. We here present Artistoo (Artificial Tissue Toolbox), a JavaScript library for building 'explorable' CPM simulations where viewers can change parameters interactively, exploring their effects in real time. Simulations run directly in the web browser and do not require third-party software, plugins, or back-end servers. The JavaScript implementation imposes no major performance loss compared to frameworks written in C++; Artistoo remains sufficiently fast for interactive, real time simulations. Artistoo provides an opportunity to unlock CPM models for a broader audience: Interactive simulations can be shared via a URL in a zero-install setting. We discuss applications in CPM research, science dissemination, open science, and education.

Data availability

Source scripts have been provided for Figure 2.

Article and author information

Author details

  1. Inge M N Wortel

    Institute for Computing and Information Sciences, Data Science, Radboud University, Nijmegen, Netherlands
    For correspondence
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-3362-5229
  2. Johannes Textor

    Department of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Nijmegen, Netherlands
    For correspondence
    Competing interests
    The authors declare that no competing interests exist.


KWF Kankerbestrijding (Young Investigator Grant,10620)

  • Johannes Textor

Nederlandse Organisatie voor Wetenschappelijk Onderzoek (Vidi Grant,192.084)

  • Johannes Textor

Radboud Universitair Medisch Centrum (Master-PhD grant)

  • Inge M N Wortel

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Andreas Buttenschoen, University of British Columbia, Canada

Publication history

  1. Received: July 21, 2020
  2. Accepted: April 8, 2021
  3. Accepted Manuscript published: April 9, 2021 (version 1)
  4. Version of Record published: May 24, 2021 (version 2)


© 2021, Wortel & Textor

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.


  • 1,753
    Page views
  • 147
  • 3

Article citation count generated by polling the highest count across the following sources: Crossref, PubMed Central, Scopus.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Open citations (links to open the citations from this article in various online reference manager services)

Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)

  1. Inge M N Wortel
  2. Johannes Textor
Artistoo, a library to build, share, and explore simulations of cells and tissues in the web browser
eLife 10:e61288.

Further reading

    1. Cell Biology
    Robert J Tower et al.
    Research Article

    De novo limb regeneration after amputation is restricted in mammals to the distal digit tip. Central to this regenerative process is the blastema, a heterogeneous population of lineage-restricted, dedifferentiated cells that ultimately orchestrates regeneration of the amputated bone and surrounding soft tissue. To investigate skeletal regeneration, we made use of spatial transcriptomics to characterize the transcriptional profile specifically within the blastema. Using this technique, we generated a gene signature with high specificity for the blastema in both our spatial data, as well as other previously published single-cell RNA-sequencing transcriptomic studies. To elucidate potential mechanisms distinguishing regenerative from non-regenerative healing, we applied spatial transcriptomics to an aging model. Consistent with other forms of repair, our digit amputation mouse model showed a significant impairment in regeneration in aged mice. Contrasting young and aged mice, spatial analysis revealed a metabolic shift in aged blastema associated with an increased bioenergetic requirement. This enhanced metabolic turnover was associated with increased hypoxia and angiogenic signaling, leading to excessive vascularization and altered regenerated bone architecture in aged mice. Administration of the metabolite oxaloacetate decreased the oxygen consumption rate of the aged blastema and increased WNT signaling, leading to enhanced in vivo bone regeneration. Thus, targeting cell metabolism may be a promising strategy to mitigate aging-induced declines in tissue regeneration.

    1. Cell Biology
    Wenyang Li et al.
    Research Article

    Chronic liver injury causes fibrosis, characterized by the formation of scar tissue resulting from excessive accumulation of extracellular matrix (ECM) proteins. Hepatic stellate cell (HSC) myofibroblasts are the primary cell type responsible for liver fibrosis, yet there are currently no therapies directed at inhibiting the activity of HSC myofibroblasts. To search for potential anti-fibrotic compounds, we performed a high-throughput compound screen in primary human HSC myofibroblasts and identified 19 small molecules that induce HSC inactivation, including the polyether ionophore nanchangmycin (NCMC). NCMC induces lipid re-accumulation while reducing collagen expression, deposition of collagen in the extracellular matrix, cell proliferation, and migration. We find that NCMC increases cytosolic Ca2+ and reduces the phosphorylated protein levels of FYN, PTK2 (FAK), MAPK1/3 (ERK2/1), HSPB1 (HSP27), and STAT5B. Further, depletion of each of these kinases suppress COL1A1 expression. These studies reveal a signaling network triggered by NCMC to inactivate HSC myofibroblasts and reduce expression of proteins that compose the fibrotic scar. Identification of the antifibrotic effects of NCMC and the elucidation of pathways by which NCMC inhibits fibrosis provide new tools and therapeutic targets that could potentially be utilized to combat the development and progression of liver fibrosis.