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People with impaired FMO3 activity either due to genetic variants known to cause trimethylaminuria or due to liver disease have reduced ability to clear TMA

6 Multiple medications have been implicated as contributing to risk of NA-AION, including amiodarone and phosphodiesterase inhibitors, though the link is controversial

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Redox-controlled reversible modifications regulate UPR signaling, for example, thiol oxidation of ER molecular chaperones such as the binding immunoglobulin protein/78-kDa glucose-regulated protein (BiP/Grp78) that enhances the release of BiP from ER stress sensors and activates UPR (Wang et al., 2014)

References Abi-Dargham A, Grace A

These findings demonstrate DOPs protective role through modulation of the gut-liver axis (139)