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explored that the FAK/p38 signaling pathways (activated) were strongly related to LIPUS intervention, and the inhibition of phosphorylated focal adhesion kinase (FAK) significantly reversed LIPUS-mediated cell proliferation, differentiation of chondrocytes, and LIPUS-mediated modulation of inflammation condition in OA mice (Sang et al., 2021)
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These secondary mechanisms are distinct from direct pharmacological effects
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