Ghrelin alleviates liver fibrosis by triggering HSCs ferroptosis via regulating injured hepatocyte-derived exosomal LncMALAT1/GPX4 pathway.

Ghrelin reduced the profibrotic effect of IHC-Exo in liver fibrosis by regulating lncMALAT1/GPX4 pathway mediated HSCs ferroptosis. Triggering HSCs ferroptosis via GHR-IHC-Exo may become a novel strategy to alleviate the progression of liver fibrosis. Liver fibrosis is the end stage of the continuous progression of a variety of chronic liver diseases. With the continuous action of various pathogenic factors, hepatic stellate cells in the liver are activated and produce a large amount of collagen fibers that are deposited in the liver, resulting in obvious damage to liver tissue and leading to cirrhosis and even liver cancer, which seriously affects human health. However, there are still clear and effective drugs approved for the treatment of liver fibrosis, so it is important to explore the possible mechanisms of liver fibrosis treatment. In previous studies, researchers found that exosomes secreted by injured hepatocytes promote the progression of liver fibrosis. In our study, we found that the role of exosomes in promoting liver fibrosis progression was attenuated after pretreatment with Ghrelin. This provides an important theoretical basis for the use of Ghrelin in the treatment of liver fibrosis.