Recently, Hou et al. shifted the research focus from the function of nuclear sirtuin (SIRT)6 to that of cytoplasmic SIRT6, which deacetylates and activates long-chain acyl-CoA synthase 5 (ACSL5). Their findings provide mechanistic insight into the role of cytoplasmic SIRT6 in fatty acid oxidation, acting as a therapeutic target for combating nonalcoholic fatty liver disease (NAFLD).
Keywords: SIRT6; deacetylation; fatty acid oxidation; lipid metabolism; long-chain acyl-CoA synthase 5; nonalcoholic fatty liver disease.
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