Does nPC1 repression contribute to lipid accumulation in human macrophages exposed to environmental aryl hydrocarbons?
Our data have shown that contaminants such as TCDD and BP repress NPC1 expression in macrophages in an AHR-dependent manner, which likely contributes to macrophage lipid accumulation caused by these environmental chemicals. Thus, NPC1 appears to be a new molecular target regulated by environmental AHs and putatively involved in their deleterious cardiovascular effects.
One-mm cancer-free resection margin achieved in patients with colorectal liver metastases should now be considered the standard of care.