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These findings support the hypothesis that glycocalyx disruption contributes to the pathophysiology of DCI through mechanisms such as neuro-inflammation, microthrombosis, endothelial dysfunction, and oxidative stress (66)

Literatures suggest a potential contribution of exosomes as a key modulator in xenobiotics- and disease-induced toxicity in various tissue systems 10,11

VDR activation suppresses oxidative damage-induced osteoblast ferroptosis through Nrf2/glutathione peroxidase 4 pathway stimulation (196) (Fig

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