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Animal model studies have preliminarily revealed that Clostridium colonization can curtail the overgrowth of pro-inflammatory microbiota, restore the intestinal mucosal barrier, and limit systemic translocation of bacterial LPS, ultimately reestablishing gut microbial homeostasis (206, 207)

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Dox-induced ER stress activates multiple pathways, including IRE1/ASK1/JNK and CHOP, contributing to inflammation, apoptosis, and autophagy [85]

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