AI Article Synopsis
- Chronic liver injury can lead to fibrosis, cirrhosis, and cancer, making it essential to find ways to prevent or reverse fibrosis.
- Hepatic stellate cells (HSCs) play a key role in fibrosis; they transform from a resting state to active myofibroblasts when the liver is injured, which increases the production of extracellular matrices.
- Researchers showed that activated HSCs could revert to a "quiescent-like" state when liver injuries are minimized and identified specific chemical compounds that can trigger this deactivation process, leading to potential new treatments for advanced liver fibrosis.
Article Abstract
Chronic liver injury induces fibrosis that often proceeds to cirrhosis and hepatocellular carcinoma, indicating that prevention and/or resolution of fibrosis is a promising therapeutic target. Hepatic stellate cells (HSCs) are the major driver of fibrosis by expressing extracellular matrices (ECM). HSCs, in the normal liver, are quiescent and activated by liver injury to become myofibroblasts that proliferate and produce ECM. It has been shown that activated HSCs (aHSCs) become a "quiescent-like" state by removal of liver insults. Therefore, deactivation agents can be a therapeutic drug for advanced liver fibrosis. Using aHSCs prepared from human induced pluripotent stem cells, we found that aHSCs were reverted to a quiescent-like state by a combination of chemical compounds that either inhibit or activate a signaling pathway, Lanifibranor, SB431542, Dorsomorphin, retinoic acid, palmitic acid and Y27632, in vitro. Based on these results, we established a high throughput system to screen agents that induce deactivation and demonstrate that a single chemical compound can induce deactivation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11014936 | PMC |
| http://dx.doi.org/10.1038/s41598-024-58989-6 | DOI Listing |
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