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• W3013874232 endingPage "441" @default.
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• W3013874232 abstract "MAFLD is the most prevalent liver disease and affects a quarter of the global population, with serious hepatic and extrahepatic consequences. The spectrum of MAFLD extends from hepatic fat accumulation to inflammation and, in some cases, to liver fibrosis and cancer. Human and animal studies indicate that MAFLD is associated with widescale alterations in the epigenetic landscape during its development and progression. Epigenetics-based drugs and editing tools are emerging as a promising therapeutic option to restore the normal (healthy) epigenetic landscape. This field has been enabled by the development of clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 technology for locus-specific epigenetic targeting. Despite decades of research, effective therapies for metabolic (dysfunction)-associated fatty liver disease (MAFLD) are lacking. An increasing body of evidence suggests that epigenetic dysregulation is frequent in MAFLD, and orchestrates many aspects of its development and progression. Furthermore, the high plasticity of epigenetic modifications in response to environmental cues renders epigenetics a novel area for therapeutic drug discovery. Over recent years, several epigenetics-based drugs and diagnostic biomarkers have entered clinical development and/or obtained regulatory approval. Here, we review recent advances in our understanding of epigenetic regulation and programming during MAFLD, including DNA methylation, histone modifications, chromatin remodelling, transcriptional control, and noncoding (nc)RNAs. We also discuss the potential translational implications and challenges of epigenetics in the context of MAFLD. Despite decades of research, effective therapies for metabolic (dysfunction)-associated fatty liver disease (MAFLD) are lacking. An increasing body of evidence suggests that epigenetic dysregulation is frequent in MAFLD, and orchestrates many aspects of its development and progression. Furthermore, the high plasticity of epigenetic modifications in response to environmental cues renders epigenetics a novel area for therapeutic drug discovery. Over recent years, several epigenetics-based drugs and diagnostic biomarkers have entered clinical development and/or obtained regulatory approval. Here, we review recent advances in our understanding of epigenetic regulation and programming during MAFLD, including DNA methylation, histone modifications, chromatin remodelling, transcriptional control, and noncoding (nc)RNAs. We also discuss the potential translational implications and challenges of epigenetics in the context of MAFLD. use of drugs or other epigenome-editing tools, such as CRISPR, to modify epigenetic control of gene expression for therapeutic purposes. represent ∼10% of all resident liver cells and are interposed between hepatocytes and liver sinusoidal endothelial cells. They are the main storage site for retinoids (vitamin A and metabolites), contained within lipid droplets. There is unequivocal evidence that activation of HSCs is the central driver of extracellular matrix deposition during the process of liver fibrosis. the most prevalent liver disease in affluent countries and a primary cause of liver cirrhosis and HCC. The spectrum of disease extends from simple steatosis [the abnormal accumulation of fat (triglyceride) in the liver] to steatohepatitis, in which triglyceride accumulation is accompanied by hepatocyte injury and inflammation, and can progress to liver fibrosis, cirrhosis, and liver cancer." @default.
• W3013874232 created "2020-04-03" @default.
• W3013874232 creator A5011865871 @default.
• W3013874232 creator A5024991274 @default.
• W3013874232 creator A5071565406 @default.
• W3013874232 creator A5083375223 @default.
• W3013874232 date "2020-06-01" @default.
• W3013874232 modified "2023-10-14" @default.
• W3013874232 title "The Epigenetic Drug Discovery Landscape for Metabolic-associated Fatty Liver Disease" @default.
• W3013874232 cites W1587676438 @default.
• W3013874232 cites W1855058198 @default.
• W3013874232 cites W1876950247 @default.
• W3013874232 cites W1960777124 @default.
• W3013874232 cites W1967041777 @default.
• W3013874232 cites W1967206613 @default.
• W3013874232 cites W1972019985 @default.
• W3013874232 cites W1981379568 @default.
• W3013874232 cites W1988128873 @default.
• W3013874232 cites W2000252175 @default.
• W3013874232 cites W2008203859 @default.
• W3013874232 cites W2009036920 @default.
• W3013874232 cites W2012154009 @default.
• W3013874232 cites W2016294119 @default.
• W3013874232 cites W2028897685 @default.
• W3013874232 cites W2032182879 @default.
• W3013874232 cites W2042194227 @default.
• W3013874232 cites W2045720893 @default.
• W3013874232 cites W2047615185 @default.
• W3013874232 cites W2048091871 @default.
• W3013874232 cites W2054504536 @default.
• W3013874232 cites W2062410076 @default.
• W3013874232 cites W2063820789 @default.
• W3013874232 cites W2064887977 @default.
• W3013874232 cites W2065467220 @default.
• W3013874232 cites W2065542401 @default.
• W3013874232 cites W2076142854 @default.
• W3013874232 cites W2084598636 @default.
• W3013874232 cites W2085436890 @default.
• W3013874232 cites W2092095172 @default.
• W3013874232 cites W2099828433 @default.
• W3013874232 cites W2105100844 @default.
• W3013874232 cites W2111357931 @default.
• W3013874232 cites W2114202720 @default.
• W3013874232 cites W2121248574 @default.
• W3013874232 cites W2121339421 @default.
• W3013874232 cites W2122607246 @default.
• W3013874232 cites W2127268992 @default.
• W3013874232 cites W2128286750 @default.
• W3013874232 cites W2134555277 @default.
• W3013874232 cites W2139342290 @default.
• W3013874232 cites W2147934487 @default.
• W3013874232 cites W2152956716 @default.
• W3013874232 cites W2162382402 @default.
• W3013874232 cites W2170135815 @default.
• W3013874232 cites W2172596207 @default.
• W3013874232 cites W2174904675 @default.
• W3013874232 cites W2175436961 @default.
• W3013874232 cites W2183645018 @default.
• W3013874232 cites W2188192437 @default.
• W3013874232 cites W2207577748 @default.
• W3013874232 cites W2290401339 @default.
• W3013874232 cites W2294327742 @default.
• W3013874232 cites W2306606423 @default.
• W3013874232 cites W2317505970 @default.
• W3013874232 cites W2337435850 @default.
• W3013874232 cites W2415515169 @default.
• W3013874232 cites W2443002311 @default.
• W3013874232 cites W2527612712 @default.
• W3013874232 cites W2533354568 @default.
• W3013874232 cites W2540412673 @default.
• W3013874232 cites W2567957521 @default.
• W3013874232 cites W2569077910 @default.
• W3013874232 cites W2584928759 @default.
• W3013874232 cites W2588510427 @default.
• W3013874232 cites W2589194866 @default.
• W3013874232 cites W2599750069 @default.
• W3013874232 cites W2600519390 @default.
• W3013874232 cites W2605366695 @default.
• W3013874232 cites W2605919588 @default.
• W3013874232 cites W2624715122 @default.
• W3013874232 cites W2739133817 @default.
• W3013874232 cites W2741636306 @default.
• W3013874232 cites W2759997926 @default.
• W3013874232 cites W2765170429 @default.
• W3013874232 cites W2765446062 @default.
• W3013874232 cites W2766316890 @default.
• W3013874232 cites W2767093292 @default.
• W3013874232 cites W2767801219 @default.
• W3013874232 cites W2768112227 @default.
• W3013874232 cites W2773119565 @default.
• W3013874232 cites W2774855547 @default.
• W3013874232 cites W2783395490 @default.
• W3013874232 cites W2785193639 @default.
• W3013874232 cites W2785571650 @default.
• W3013874232 cites W2787895823 @default.
• W3013874232 cites W2793833249 @default.
• W3013874232 cites W2802858168 @default.
• W3013874232 cites W2803248842 @default.

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