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• W3013902547 abstract "To the Editor: We read with interest the recent article by Kumar et al.(1) on the impact of augmenter of liver regeneration (ALR) deficiency on nonalcoholic fatty liver disease (NAFLD) progression from steatosis to nonalcoholic steatohepatitis (NASH). By using hepatocyte-specific ALR knockout/knockdown high-fat/high-carbohydrate mouse models, they demonstrated an involvement of ALR in lipid metabolism, oxidative stress, and inflammatory response leading to fibrosis. However, ALR is expressed in three isoforms (15, 21, 23 kDa),(2) and their specific roles in this “loss-of-function” strategy is not addressed. In earlier publications, using an overexpression approach (“gain-of-function”) of the mainly mitochondrial 23-kDa ALR, a reduction in hepatic fibrosis and ischemia reperfusion injury (IRI) in steatotic livers was shown.(2) Expression of cytosolic 15-kDa ALR reduced severity of liver injury in a methionine-choline–deficient NASH mouse model.(2) Furthermore, it was shown that cytosolic 15-kDa ALR, different from exogenously applied 15-kDa ALR, diminished triacylglycerol levels and lipoapotosis in vitro by attenuating endoplasmatic stress, increasing lipolytic and decreasing lipogenic gene expression.(3) Additionally, treatment with exogenous ALR reduced hepatic IRI in mice by reducing neutrophil infiltration through less hepatocytic chemokine expression.(4) More detailed knowledge of the function of individual ALR isoforms is necessary for future therapeutic interventions. Kumar et al. found decreased ALR levels in human NASH patients (tissue and serum) and pointed to a lack of information about ALR regulation. This was addressed earlier, demonstrating reduced hepatic ALR mRNA levels in patients with steatosis and even more with NASH.(2, 3) ALR is regulated, among others, by forkhead box A2 (FOXA2; hepatocyte nuclear factor 3β), which translocates from the nucleus to the cytosol upon treatment with free fatty acids, and whose expression correlates with ALR expression in NAFLD patients.(3) Nuclear factor erythroid 2–related factor 2 (Nrf2), another ALR-regulating transcription factor,(2) was shown to attenuate liver steatosis and therefore it is likely that FOXA2 and Nrf2 diminished endogenous ALR levels in hepatic steatosis/NASH. However, the conclusion that ALR deficiency may be a major determinant of accelerated progression of NASH to end-stage liver disease, that is, cirrhosis, is not supported by enhanced ALR levels in patients with cirrhosis(2) or by clinical characterization of patients with mutations in the growth factor erv1-like (GFER) gene (encoding for ALR) showing almost no distinctive feature regarding hepatic function(2) and therefore should to be taken with caution." @default.
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• W3013902547 date "2020-09-01" @default.
• W3013902547 modified "2023-09-26" @default.
• W3013902547 title "Letter to the Editor: Does Augmenter of Liver Regeneration Deficiency Pave the Way for Nonalcoholic Steatohepatitis Progression?" @default.
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• W3013902547 doi "https://doi.org/10.1002/hep.31248" @default.
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