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Liver Regeneration

Liver Regeneration

The liver is an important organ in vertebrates that plays an essential role in metabolism. It is also responsible for storing and redistributing nutrients such as carbohydrates, fats, and vitamins in the body. Additionally, the liver releases bile salts which are critical for digesting food and eliminating toxic metabolites from the body.
Cells of Liver
The liver comprises four major types of cells— hepatocytes, stellate, Kupffer, and sinusoidal endothelial cells. The hepatocytes are...

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Ghrelin alleviates liver fibrosis by triggering HSCs ferroptosis via regulating injured hepatocyte-derived exosomal

Xin Luo¹, Kan Chen², Jie Zhang²

¹Department of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology

|January 21, 2025

Summary

Ghrelin pretreatment mitigates liver fibrosis by targeting injured hepatocyte-derived exosomes (IHC-Exo). This approach regulates the lncMALAT1/GPX4 pathway, inducing ferroptosis in hepatic stellate cells (HSCs) and offering a novel therapeutic strategy.

Keywords:

exosomes ferroptosis ghrelin liver fibrosis lncMALAT1

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Area of Science:

Hepatology
Molecular Biology
Cellular Biology

Background:

Liver fibrosis, a severe consequence of chronic liver diseases, involves activated hepatic stellate cells (HSCs) depositing excessive collagen.
Current treatments for liver fibrosis lack efficacy, necessitating exploration of novel therapeutic mechanisms.
Exosomes derived from injured hepatocytes (IHC-Exo) have been identified as promoters of liver fibrosis progression.

Purpose of the Study:

To investigate the potential of Ghrelin in attenuating liver fibrosis.
To elucidate the molecular mechanisms by which Ghrelin affects IHC-Exo-induced liver fibrosis.
To explore the role of HSC ferroptosis in Ghrelin's therapeutic effect.

Main Methods:

Investigated the effect of Ghrelin pretreatment on IHC-Exo in a liver fibrosis model.
Analyzed the regulation of the long non-coding RNA MALAT1 (lncMALAT1) and glutathione peroxidase 4 (GPX4) pathway.
Assessed the induction of ferroptosis in hepatic stellate cells (HSCs).

Main Results:

Ghrelin pretreatment significantly reduced the profibrotic effects of IHC-Exo.
Ghrelin modulated the lncMALAT1/GPX4 pathway, a key regulator of ferroptosis.
Ghrelin treatment promoted ferroptosis in HSCs, thereby alleviating liver fibrosis.

Conclusions:

Ghrelin effectively counteracts the profibrotic impact of IHC-Exo in liver fibrosis.
Targeting the lncMALAT1/GPX4 pathway and inducing HSC ferroptosis via Ghrelin presents a promising therapeutic avenue.
Ghrelin's ability to attenuate liver fibrosis progression offers a novel strategy for clinical consideration.