The team used these models to show drug responses and established a CRISPR-screening platform to identify potential therapeutic targets for non-alcoholic fatty liver disease.
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non-alcoholic fatty liver disease (NAFLD)
The researchers used single-nuclear sequencing and advanced three-dimensional glass imaging of mice to find new drug targets for non-alcoholic fatty liver disease.
Researchers have presented comprehensive multi-omic profiles to identify genes, non-coding RNAs, proteins, and plasma metabolites involved in NAFLD-to-NASH progression.
DNA methylation at specific genomic sites was found to correlate with non-fatty liver disease and could be used to diagnose severity.
Researchers have successfully used label-free near-infrared hyperspectral imaging for mouse livers, which could aid in the diagnosis of NAFLD.
A liver-on-a-chip model has been developed to more fully represent the natural progression of NAFLD than previous models.
The patient-derived model of non-alcoholic fatty liver disease (NAFLD) accurately reproduced the complex human metabolic pathways involved in the development of the disease.
Current state of NAFLD treatments and the promise of in vitro platforms towards better screening of drug candidates
The heterogeneous pathogenesis of metabolic fatty liver diseases presents researchers with numerous challenges when trying to develop a treatment. This article explores the spectrum of these diseases and presents a novel in vitro platform for screening drug candidates.
The novel peripheral serotonin antagonist, based on Parkinson’s drug pimavanserin, increased glucose tolerance and lean body mass in a murine model of non-alcoholic fatty liver disease (NAFLD).
Included in this in-depth focus are articles on how high-throughput screening can be used to identify lead compounds, using chemoinformatics as a map to guide drug discovery and a novel in vitro model to screen potential treatments for non-alcoholic fatty liver disease (NAFLD).
A study identifying transcription factor differences in the hepatic stellate cells of mice with liver fibrosis named PPARγ as a potential target for the condition’s regression and scar resolution therapies.
New lab on a chip technology has been developed to evaluate the effects of different drivers of NAFLD on liver cells.