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The role of oxidative stress in the COVID-19 disease may involve recognition of the viral S-protein by angiotensin converting enzyme-2 (ACE2) receptor and pattern recognition receptors like toll-like receptors 2 and 4, and activation of transcription factors like nuclear factor kappa B, that subsequently activate nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) expression succeeded by ROS production (Kozlov et al., 2021)
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The primary mechanisms through which BPC-157 promotes tissue repair include activation of the VEGFR2 signaling pathway for angiogenesis (new blood vessel formation), FAK-paxillin pathway activation that enhances cell migration to injury sites, upregulation of growth hormone receptors that amplify proliferative signals, and selective modulation of nitric oxide systems that balance beneficial vasodilation against inflammatory damage
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