HMGB1 and metabolic dysfunction-associated steatotic liver disease: Rabadi et al. (2015) have also demonstrated that the inflammation-induced suppression of SIRT1 inhibits HMGB1 deacetylation and promotes its nuclear-to-cytoplasmic translocation and systemic secretion, therefore keeping inflammation. Meng et al. (2020) indicate that salvianolic acid B (SalB), can suppress the relocation and secretion of HMGB1 by upregulating SIRT1 in the liver parenchymal cells during NAFLD. Meanwhile, SIRT1-mediated deacetylation can result in the resveratrol-mediated suppression of HMGB1 nuclear-to-cytoplasmic translation in sepsis-induced liver injury (Xu et al., 2014).