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Non-alcoholic fatty liver disease (NAFLD) represents the most common hepatic manifestation of chronic liver diseases in developed countries. Since non-alcoholic steatohepatitis (NASH) is responsible for a large proportion of cryptogenic cirrhosis and cirrhosis represents the main risk factor for hepatocellular carcinoma (HCC), HCC is a severe complication of end-stage NAFLD.1
Recent evidence published in this journal showed the therapeutic potential of an inhibition of the chemokine (C-C motif) ligand 2 (CCL2)/monocyte chemoattractant protein-1 (MCP-1) in NASH.2 The study by Baeck et al elegantly demonstrated that the pharmacological administration of an RNA oligonucleotide against MCP-1 ameliorates murine steatosis and inflammation. Since mice deficient of the MCP-1 receptor also showed attenuated fibrosis, MCP-1 was suggested as a critical link in the axis steatosis–inflammation–fibrosis.2
Here, we report that animals with a liver-specific overexpression of the insulin-like growth factor 2 (IGF2) mRNA-binding protein p62/IMP2-2/IGF2BP2-2 exhibit distinctly elevated Ccl2 expression levels (figure 1A) when fed a methionine–choline-deficient (MCD) diet, which models all hepatic stages of NAFLD. Accordingly, in addition to elevated inflammatory gene expression, p62 transgenics had higher fat deposition (figure 1B) …
Footnotes
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Collaborators Eva Dilly; Christina Guth.
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Contributors YS, SMK and AKK designed experiments, analysed data and wrote the manuscript. AKK initiated and directed the study. SMK, RMB and JH scored the histological slides.
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Funding The project was funded in part by an EASL Sheila Sherlock and a Bank Austria Visiting Scientists Program Fellowship to SMK.
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Competing interests None.
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Provenance and peer review Not commissioned; internally peer reviewed.
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Data sharing statement All authors had full access to all of the data (including statistical reports and tables) in the study and can take responsibility for the integrity of the data and the accuracy of the data analysis.