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The myotendinous junction studies (Japjec et al., 2021, Biomedicines ) extended the tendon work to the muscle-tendon interface, showing accelerated healing of disabled junctions in rats

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Interestingly, matrix metalloproteinases, pro-inflammatory cytokines, oxidative stress and mitochondrial dysfunction are the potential factors triggering neuro-inflammation resulting in neural dysfunction all of which are involved in ASD pathogenesis

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