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This significantly elevates Angiotensin II (Ang II) levels, a key RAAS mediator, which induces intestinal epithelial injury through four main pathways: (1) Ang II selectively inhibits P-glycoprotein (Pgp) function and membrane expression in intestinal epithelial cells via AT1 receptor-mediated PI3K/Akt-p38 MAPK signaling

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4A), and the results revealed an upregulation of IRE1 (an ER stress marker), indicating ER stress activation, reduced p62 levels, and increased LC3BII levels within 012 h of PFOS treatment