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IL-17A promotes lung fibrosis through impairing mitochondrial homeostasis in type II alveolar epithelial cells

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The GSH synthetic pathway is illustrated in Fig

In AD, however, tau undergoes pathological hyperphosphorylation, leading to its dissociation from microtubules, aggregation into neurofibrillary tangles, and ultimately neuronal dysfunction (1)

When this system is functioning optimally, heavy metals and oxidative byproducts are cleared before they can accumulate in tissues and cause cellular damage