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Endoplasmic reticulum stress and iron homeostasis: a new frontier of the universal periodic review

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Document pages: 10 pages

Abstract: The C282Y mutation of HFE accounts for the majority of cases of iron overload disease hereditary hemochromatosis (Hh).e ER stress stimuli, was shown to reshape the expression profile of iron-related genes and to decrease MHC-I cell surface expression. The possibility of a HFE-C282Y-mediated interplay between the UPR and iron homeostasis influencing disease progression and the clinical heterogeneity among C282Y carriers is discussed. The responsiveness of the ER chaperone calreticulin to both ER and iron-induced oxidative stresses, and its correlation with HH patients’ phenotype, reinforce the interest of dissecting the UPR signaling iron metabolism crosstalk and points to the potential clinical value of use of pharmacological chaperones in HFE-HH.

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