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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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The mechanical utilization of contractile force produced by myofilaments efficiently connected to tendon fibers as a follow up of the BPC 157 therapy was successfully achieved (i.e., recovery of the myotendinous junction and its function following dissection of quadriceps tendon from quadriceps muscle) [43]
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