Biomaterials as Regulators of Neuron–Glia Crosstalk: From Material Properties to Functional Outcomes
4 affiliations
- 1Scientific Center for Genetics and Life Sciences, Sirius University of Science and Technology, 1, Olympic Ave., 354340 Sochi, Russia
- 2Institute of Translational Biomedicine, St. Petersburg State University, 199034 St. Petersburg, Russia
- 3Moscow Center for Advanced Studies, 20, Kulakova Str., 123592 Moscow, Russia
- 4Pavlov Institute of Physiology, Russian Academy of Sciences, 199034 St. Petersburg, Russia
Abstract
Biomaterials for neural tissue engineering, cell delivery, and chronic neural interfaces are conventionally characterized through physicochemical descriptors such as stiffness, topography, surface chemistry, and degradation rate. However, their biological effects are mediated by the material–tissue interface, which evolves through protein adsorption, extracellular matrix ligand presentation, and progressive cellular remodeling and determines how these design parameters are translated into neuronal and glial responses. This review synthesizes current evidence on how neurons, astrocytes, and microglia sense the material–tissue interface, how integrin-dependent adhesion complexes, mechanosensitive Piezo1 channels, and downstream FAK/Src, RhoA/ROCK, and YAP/TAZ pathways transduce interfacial cues into intracellular signaling, and how key design variables (mechanical properties, architecture, surface chemistry, electrical conductivity, and degradation) can be tuned to direct these processes in regenerative scaffolds and chronic neural interfaces. Particular attention is given to studies distinguishing direct neuronal effects from glia-mediated modulation, since concurrent changes in neuronal and glial markers are often reported without establishing causal neuron–glia interaction. We further discuss methodological limitations that constrain current interpretations of biomaterial-induced neuron–glia crosstalk, including discrepancies between 2D, 3D, and in vivo models and insufficient durations of chronic observation. We argue that functional biomaterial design for neural applications should move from optimizing isolated cellular readouts toward multicellular experimental frameworks capable of resolving neuron–glia–ECM interactions over physiologically relevant timescales.
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BibTeX
@article{shtol2026biomaterials,
title = {{Biomaterials as Regulators of Neuron–Glia Crosstalk: From Material Properties to Functional Outcomes}},
author = {Valeriia S. Shtol and Sophia P. Konovalova and Kirill A. Arsentiev and Yulia I. Taranukha and Pavel E. Musienko},
journal = {Cells},
year = {2026},
month = nov,
doi = {10.3390/cells15212019},
url = {https://www.mdpi.com/2073-4409/15/21/2019},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Biomaterials as Regulators of Neuron–Glia Crosstalk: From Material Properties to Functional Outcomes
AU - Valeriia S. Shtol
AU - Sophia P. Konovalova
AU - Kirill A. Arsentiev
AU - Yulia I. Taranukha
AU - Pavel E. Musienko
PY - 2026
DA - 2026/11/05
JO - Cells
DO - 10.3390/cells15212019
UR - https://www.mdpi.com/2073-4409/15/21/2019
AB - Biomaterials for neural tissue engineering, cell delivery, and chronic neural interfaces are conventionally characterized through physicochemical descriptors such as stiffness, topography, surface chemistry, and degradation rate. However, their biological effects are mediated by the material–tissue interface, which evolves through protein adsorption, extracellular matrix ligand presentation, and progressive cellular remodeling and determines how these design parameters are translated into neuronal and glial responses. This review synthesizes current evidence on how neurons, astrocytes, and microglia sense the material–tissue interface, how integrin-dependent adhesion complexes, mechanosensitive Piezo1 channels, and downstream FAK/Src, RhoA/ROCK, and YAP/TAZ pathways transduce interfacial cues into intracellular signaling, and how key design variables (mechanical properties, architecture, surface chemistry, electrical conductivity, and degradation) can be tuned to direct these processes in regenerative scaffolds and chronic neural interfaces. Particular attention is given to studies distinguishing direct neuronal effects from glia-mediated modulation, since concurrent changes in neuronal and glial markers are often reported without establishing causal neuron–glia interaction. We further discuss methodological limitations that constrain current interpretations of biomaterial-induced neuron–glia crosstalk, including discrepancies between 2D, 3D, and in vivo models and insufficient durations of chronic observation. We argue that functional biomaterial design for neural applications should move from optimizing isolated cellular readouts toward multicellular experimental frameworks capable of resolving neuron–glia–ECM interactions over physiologically relevant timescales.
SN - 2073-4409
ER -