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Microglia cells would amp up the inflammatory response and release inflammatory cytokines and chemokines, which would result in neuronal death [60, 61]

Up to now, in addition to mitochondrial oxidative stress, many other cellular processes, including phase I/phase II metabolism, endoplasmic reticulum stress, autophagy, sterile inflammation, microcirculatory dysfunction, and liver regeneration, have been identified to be involved in the pathogenesis of AILI, providing new targets for developing more effective therapeutic interventions against APAP-induced liver injury

Rbsam, A

Decoding SARS-CoV-2 hijacking of host mitochondria in COVID-19 pathogenesis