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Fig. 7 Overall proposed model of the therapeutic mechanism of FBLN5 in myelin-related diseases. Proper development of Schwann cells through the processes of proliferation, elongation, and myelination is essential for the functioning of the PNS. The common pathological symptom of dysmyelinating and demyelinating diseases is uncompact myelin ensheathments of the axons. Our findings suggest that FBLN5 secreted from MSCs or recombinant FBLN5 present in the ECM binds to the Integrin receptors and promotes actin remodeling through RAC1 activation in the Schwann cells. Then, the Schwann cells are recovered by an activated actin remodeling mechanism and induce the compact myelination of the diseased axons