ArticleBiophysical journal2022
Unified multiscale theory of cellular mechanical adaptations to substrate stiffness.
Article in Biophysical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Substrate elasticity controls fibroblast motility on non-oxidized PDMS under weak adhesion.Biophysics and physicobiology · 2026Article
- Chemical compensation to mechanical loss in cell mechanosensation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Adhesion-regulated dynamics of cells.Biophysical journal · 2025Article
- Elastic interactions compete with persistent cell motility to drive durotaxis.Biophysical journal · 2024Article
- Selective Suppression of Integrin-Ligand Binding by Single Molecular Tension Probes Mediates Directional Cell Migration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Directional Cell Migration Guided by a Strain Gradient.Small (Weinheim an der Bergstrasse, Germany) · 2024Article
- A multiscale theory for spreading and migration of adhesion-reinforced mesenchymal cells.Journal of the Royal Society, Interface · 2023Article
- Understanding How Cells Probe the World: A Preliminary Step towards Modeling Cell Behavior?International journal of molecular sciences · 2023Article
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Authors and funding
3 authors.
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Abstract
Rigidity of the extracellular matrix markedly regulates many cellular processes. However, how cells detect and respond to matrix rigidity remains incompletely understood. Here, we propose a unified two-dimensional multiscale framework accounting for the chemomechanical feedback to explore the interrelated cellular mechanosensing, polarization, and migration, which constitute the dynamic cascade in cellular response to matrix stiffness but are often modeled separately in previous theories. By combining integrin dynamics and intracellular force transduction, we show that substrate stiffness can act as a switch to activate or deactivate cell polarization. Our theory quantitatively reproduces rich stiffness-dependent cellular dynamics, including spreading, polarity selection, migration pattern, durotaxis, and even negative durotaxis, reported in a wide spectrum of cell types, and reconciles some inconsistent experimental observations. We find that a specific bipolarized mode can determine the optimal substrate stiffness, which enables the fastest cell migration rather than the largest traction forces that cells apply on the substrate. We identify that such a mechanical adaptation stems from the force balance across the whole cell. These findings could yield universal insights into various stiffness-mediated cellular processes within the context of tissue morphogenesis, wound healing, and cancer invasion.
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