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The zonulin-induced disruption of the tight junction complex allows paracellular transport of gliadin and the eventual uptake of gliadin into systemic circulation, thereby causing the inflammatory response exhibited by patients with celiac disease (26, 34, 35)

Our data further suggest that autologous fibroblasts can induce native NP cells in degenerative IVDs to adopt a fibrotic phenotype via the activation of TGF/Smad signaling in order to enhance the reparative fibrosis and healing process (Fig

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