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An emerging hypothesis proposes that vascular dysfunction in CFLD may arise from exaggerated inflammatory responses of the portal endothelium to gut derived pathogen-associated molecular patterns (PAMPs), or alternatively from CFTR-related defects in endothelial cells themselves, possibly compounded by inflammatory signals originated from the inflamed biliary epithelium (Fiorotto Romina, unpublished data ) (Figure 1)

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The metabolic waste ammonium regulates mTORC2 and mTORC1 signaling