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Inflammation and pyroptosis mediate substantial epithelial and endothelial injury with a subsequent loss of the alveolar-capillary barrier integrity, leading to influx of protein-rich edema fluid and immune cells into the alveoli [2]

The answer may lie in a naturally occurring molecule that plays a critical role in cellular repair and regeneration

A slightly oxidative environment also helps preserve sensitive norisoprenoids, such as -damascenone, although thiols may be diminished through oxidative degradation

This resistance indicates the existence of evolved mechanisms that are able to evade surveillance