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95,96 Excessive endoplasmic reticulum stress leads to an increase in trypsin activity, which in turn stimulates PAR2 and PAR4 receptors, increases intestinal permeability, destroys the function of the intestinal barrier, and promotes the development of inflammatory processes

The FB1 causes autophagic cell death in MARC-145 monkey kidney cells, and the research of FB1-induced toxicities by altered sphingolipid metabolism found that this disruption of sphingolipid metabolism is an essential first step (84)

Our results demonstrate that GC potentiates CMA activity in macrophages, leading to promoted degradation of the NLRP3 inflammasome, suppression of NLRP3/IL-1-mediated inflammation, and ultimately conferring protection against atherosclerosis

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