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The homocysteine-inducible, endoplasmic reticulum (ER) stress-inducible, ubiquitin-like domain member 2 (HERPUD1) in cultured HELA cells facilitate cytoprotective effects against oxidative stress by suppressing the inositol 1,4,5-triphosphate receptor and reducing the transfer of calcium ions from the endoplasmic reticulum to mitochondria [41]
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In addition, TMAO also activated proteinase C, and induced functional damage of vascular endothelial cells through the PKC/NF-B pathway