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Activating FGFR1 restores Integrin-β1--mediated fibronectin sensing in satellite cells of aged mice

Chang, T.-L.; Vallery, T. K.; Zlatkov, T. S.; Cutler, A. A.; Kurland, J. V.; Butcher, C. H.; Anseth, K. S.; Olwin, B. B.

2026-02-19 cell biology
10.64898/2026.02.18.706475 bioRxiv
Show abstract

Muscle satellite cells (SCs), essential for skeletal muscle regeneration, decline in number and function with age, contributing to sarcopenia. A fully defined viscoelastic hydrogel that preserves SC-myofiber interactions and supports tunable densities of fibronectin-derived RGD ligands was used to investigate age-related defects in extracellular matrix sensing by SCs. Elevating RGD density increased the number of activating and proliferating SCs on myofibers from young mice, whereas SCs from aged mice were unresponsive. Loss of FGF receptor 1 signaling in SCs from aged mice abrogated the coordinated Syndecan-4 and Integrin-{beta}1 matrix response observed in SCs from young mice. Activating Integrin-{beta}1 promoted asymmetric division and self-renewal in SCs from young mice whereas combined FGFR1 and Integrin-{beta}1 signaling drove symmetric expansion. In SCs from aged mice, FGFR1 dysfunction disrupted this balance, impairing asymmetric division, but constitutive FGFR1 activation restored receptor co-localization, self-renewal, and fibronectin responsiveness. Therefore, FGFR1 integrates matrix and growth factor signals, suggesting that targeting the FGFR1-Integrin-{beta}1 axis may enhance SC regenerative potential in aging organisms.

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"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.