AI Article Synopsis
- * The mechanisms behind liver fibrosis are complex and mainly start in liver cells (hepatocytes), but are still not fully understood despite many studies.
- * A study in the JCI highlights a specific pathway (ATF3/HES1/CEBPA/OPN) that connects signals from hepatocytes to the activation of cells leading to fibrosis, suggesting potential new treatment strategies for liver fibrosis caused by MASLD.
Article Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) affects nearly 40% of the global adult population and may progress to metabolic dysfunction-associated steatohepatitis (MASH), and MASH-associated liver fibrosis and cirrhosis. Despite numerous studies unraveling the mechanism of hepatic fibrogenesis, there are still no approved antifibrotic therapies. The development of MASLD and liver fibrosis results from complex cell-cell interactions that often initiate within hepatocytes but remain incompletely understood. In this issue of the JCI, Yan and colleagues describe an ATF3/HES1/CEBPA/OPN pathway that links hepatocyte signals to fibrogenic activation of hepatic stellate cells and may provide new perspectives on therapeutic options for MASLD-induced liver fibrosis.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10977975 | PMC |
| http://dx.doi.org/10.1172/JCI179710 | DOI Listing |
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