Key result
Genetic variation predisposing to NASH and fibrosis differs markedly from simple steatosis, with substantial overlap in biological pathways between the mouse model and human disease.
Distinct genetic factors are involved in the progression from simple steatosis to NASH and fibrosis, with substantial overlap in biological pathways between a humanized mouse model and human disease.
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Does not yet alter NAFLD management; leaves open whether shared pathways offer new human drug targets.
Hui et al. (2018) studied Nonalcoholic steatohepatitis (NASH) and fibrosis. Genetic background and Western diet was evaluated on Genetic loci and biological pathways contributing to steatosis and NASH. Genetic variation predisposing to NASH and fibrosis differs markedly from simple steatosis, with substantial overlap in biological pathways between the mouse model and human disease.
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