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The activation of macrophages within plaques is driven by a complex interplay of pro-inflammatory signals, oxidative stress, and maladaptive immune responses, creating a vicious cycle of inflammation and tissue damage

Experimental models of anoxia/reoxygenation injury demonstrated that larazotide preserves epithelial barrier integrity by maintaining transepithelial electrical resistance and preventing the disassembly of tight junction components such as ZO-1, occludin, and claudins