Health
Discovery of therapeutic drug target for non-alcoholic fatty liver disease
Single-nucleus sequencing of mouse and human liver tissue and advanced 3D glass imaging in mice are used to characterize hepatocytes that generate significant scarring. (NAFLD).
as a result,”An autocrine signaling circuit in hepatic stellate cells underlies advanced fibrosis in nonalcoholic steatohepatitiswas published in Science Translational Medicinewhich may lead to new treatments.
“Advanced liver fibrosis caused by activation of hepatic stellate cells (HSCs) affects millions of people worldwide and is the leading cause of mortality in non-alcoholic steatohepatitis (NASH). It is the strongest predictor, but there is no approved antifibrotic therapy,” the researchers wrote. “Using mononuclear RNA-sequencing and tissue ablation in a robust mouse NASH model to identify antifibrotic drug targets, the progressive transcriptome and morphology associated with HSC activation in progressive disease I have combined the responses.”
The researchers performed single-nucleus sequencing in parallel studies of both mouse models of NASH and human liver tissue from nine subjects and two controls with NASH. They identified a shared number of 68 pairs of potential drug targets across the two species.
“By understanding the basis of this fibrous scarring and studying hepatic stellate cells, we aimed to identify drug targets that could lead to new treatments for advanced NASH. Arthur M. Fishberg, M.D., Dean of Therapeutic Discovery, and Head of the Liver Disease Division at Icahn Mount Sinai: “This novel grass river imaging approach—an advanced tissue clearing technique that allows for deep insight—can be applied to individual astrocytes. Combined with the gene expression analysis of , we have uncovered a completely new understanding of how these cells generate scars as NASH progresses to late stages.”
“We confirmed the importance of one such protein pair, NTF3-NTRK3, using a molecule already developed to block NTRK3 in human cancers, which has been shown to reduce NASH fibrosis and We reused it to establish its potential as a new drug to fight,” said lead author Shuang (Sammi ) Wang, PhD, instructor in the Department of Liver Disease. “This new understanding of fibrosis development suggests that advanced fibrosis may have a unique repertoire of signals that accelerate scarring, representing a previously unrecognized set of drug targets. suggests.”
Researchers are now working with chemists at Icahn Mount Sinai to further optimize NTRK3 inhibitors for the treatment of liver fibrosis. They hope to extend efforts to determine whether similar interactions between fibrogenic cells underlie fibrosis in other tissues, including heart, lung, and kidney.
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