# MASH and the race for liver antifibrotics

## TL;DR

This paper discusses new treatments for liver fibrosis in MASH and other chronic liver diseases, focusing on metabolic therapies and future directions.

## Contribution

The paper provides an overview of emerging antifibrotic therapies and considers future treatment combinations and patient stratification strategies.

## Key findings

- Metabolic therapies like GLP-1 analogues and THRβ activators show promise in reducing liver fibrosis.
- Non-metabolic antifibrotic drug development is progressing more slowly.
- Future research should explore therapeutic combinations and whether fibrosis reversal is the only goal.

## Abstract

Metabolic dysfunction-associated steatohepatitis (MASH), along with other chronic liver diseases, leads to progressive fibrosis and, ultimately, cirrhosis. Liver fibrosis is a major cause of global morbidity and mortality. Although past efforts to develop antifibrotic drugs have largely failed, recent advances in MASH metabolic therapies offer new hope. These include both indirect-acting agents such as glucagon-like peptide 1 (GLP-1) analogues, which reduce liver fat by promoting weight loss, and therapies with direct-acting mechanisms on the liver, such as thyroid hormone receptor beta (THRβ) activators and fibroblast growth factor 21 (FGF21) analogues. This perspective summarises emerging antifibrotics, from the fast-evolving class of metabolic therapies through to the more sluggish development of non-metabolic antifibrotics. We consider future therapeutic combinations and patient stratifiers that may impact patient outcomes, and close by asking if fibrosis reversal should be the only goal.