ArticleNature communications2022
Feedback between mechanosensitive signaling and active forces governs endothelial junction integrity.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Single Cell Mechanics in Disease Progression.Small science · 2026Review
- A continuous-discrete model of cell contraction incorporating actin and intermediate filaments.iScience · 2026Article
- Pulsatile flow dynamics maintain pulmonary artery architecture.JCI insight · 2026Article
- Nuclear Mechanotransduction Across the Metastatic Cascade: Decoding Spatiotemporal Heterogeneity in Cancer Dissemination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- VE-Cadherin-Actin Regulation Promotes Mechanotransduction and Monolayer Maturation Involving a Tension-Sensitive Intermediate State.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- VE-cadherin interaction proteomics identifies ARVCF as stabilizer of endothelial adherens junctions.iScience · 2026Article
- Actin-membrane interface stress regulates Arp2/3-branched actin density during lamellipodial protrusion.bioRxiv : the preprint server for biology · 2026Article
- Controlling tissue size by active fracture.Physical review. E · 2026Article
- Endothelial Klf9 fine-tunes Akt signaling to act as a transcriptional brake restraining retinal angiogenesis.International journal of biological sciences · 2026Article
- A systematic investigation of endothelial cell behavior under hydrostatic pressure.Scientific reports · 2025Article
- Bonding under tension: Some cadherins are better than others.Biophysical journal · 2025Article
- Cadherin dynamics and cortical tension in remodeling cell-cell adhesion during EMT.Biophysical journal · 2025Article
- Article
- Bioprinting of Aptamer-Based Programmable Bioinks to Modulate Multiscale Microvascular Morphogenesis in 4D.Advanced healthcare materials · 2025Article
- Confinement, Jamming, and Adhesion in Cancer Cells Dissociating from a Collectively Invading Strand.PRX life · 2025Article
- Multi-stage mechanisms of tumor metastasis and therapeutic strategies.Signal transduction and targeted therapy · 2024Review
- Magnetogenetics as a promising tool for controlling cellular signaling pathways.Journal of nanobiotechnology · 2024Review
- UV-Triggered Hydrogel Coating of the Double Network Polyelectrolytes for Enhanced Endothelialization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Discrete network models of endothelial cells and their interactions with the substrate.Biomechanics and modeling in mechanobiology · 2024Article
- Active viscoelastic models for cell and tissue mechanics.Royal Society open science · 2024Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
The formation and recovery of gaps in the vascular endothelium governs a wide range of physiological and pathological phenomena, from angiogenesis to tumor cell extravasation. However, the interplay between the mechanical and signaling processes that drive dynamic behavior in vascular endothelial cells is not well understood. In this study, we propose a chemo-mechanical model to investigate the regulation of endothelial junctions as dependent on the feedback between actomyosin contractility, VE-cadherin bond turnover, and actin polymerization, which mediate the forces exerted on the cell-cell interface. Simulations reveal that active cell tension can stabilize cadherin bonds, but excessive RhoA signaling can drive bond dissociation and junction failure. While actin polymerization aids gap closure, high levels of Rac1 can induce junction weakening. Combining the modeling framework with experiments, our model predicts the influence of pharmacological treatments on the junction state and identifies that a critical balance between RhoA and Rac1 expression is required to maintain junction stability. Our proposed framework can help guide the development of therapeutics that target the Rho family of GTPases and downstream active mechanical processes.
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