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- W4313117118 startingPage "51" @default.
- W4313117118 abstract "The liver is the most important organ that metabolizes and detoxifies chemicals taken into the body. Therefore, there is always a risk of liver damage owing to the toxic effects of chemicals. The mechanisms of hepatotoxicity have been studied extensively and deeply based on toxic effects of chemicals themselves. However, it is important to note that liver damage is variously modified by the patho-biological reactions evoked mainly via macrophages. Macrophages appearing in hepatotoxicity are evaluated by the M1/M2 polarization; M1 macrophages promote tissue injury/inflammation, whereas M2 macrophages show anti-inflammatory action including reparative fibrosis. The portal vein-liver barrier regulated by Kupffer cells and dendritic cells in and around the Glisson's sheath may be related to the initiation of hepatotoxicity. In addition, Kupffer cells exhibit the two-sides of functions (that is, M1 or M2 macrophage-like functions), depending on microenvironmental conditions which may be raised in part by gut microbiota-derived lipopolysaccharide. Furthermore, damage-associated molecular patterns (DAMPs) (in particular, HMGB1) and autophagy (which degrades DAMPs) also play roles in the polarity of M1/M2 macrophages. The mutual relation of DAMPs (HMGB-1)-autophagy-M1/M2 macrophage polarization as the patho-biological reaction should be taken into consideration in hepatotoxicity evaluation." @default.
- W4313117118 created "2023-01-06" @default.
- W4313117118 creator A5009514473 @default.
- W4313117118 creator A5035550385 @default.
- W4313117118 creator A5035894974 @default.
- W4313117118 date "2023-01-01" @default.
- W4313117118 modified "2023-09-25" @default.
- W4313117118 title "Macrophage pathology in hepatotoxicity" @default.
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