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Mechanism of coronavirus-induced neuronal damage via oxidative stress and mitochondria dysfunction
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Description
Coronavirus infects via TMPRSS2 priming of the spike proteins, enabling ACE2 binding. The affinity interaction triggers the binding of Ang II to the angiotensin type 1 receptor (AT1R), activating NADPH oxidase. This leads to mitochondrial electron transport chain (ETC) damage via the release of oxidative and nitrosative species, subsequently increasing the formation of mitochondrial reactive oxygen species (mtROS) and inflammatory cytokines, which can compromise the blood–brain barrier.
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