# Peroxisome Proliferator-Activated Receptor β/δ: A Link Between Metabolism, Inflammation, and Fibrosis in Metabolic Dysfunction-Associated Steatotic Liver Disease

## TL;DR

This paper reviews how PPARβ/δ helps prevent liver disease by improving metabolism and reducing inflammation and fibrosis.

## Contribution

The paper provides a comprehensive review of PPARβ/δ's role in MASLD progression and its molecular mechanisms.

## Key findings

- PPARβ/δ is expressed in key liver cells and may prevent MASLD progression.
- PPARβ/δ reduces insulin resistance, lipotoxicity, and inflammation in liver disease.
- The receptor also attenuates fibrosis associated with metabolic dysfunction.

## Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is considered a hepatic manifestation of insulin resistance and ranges from isolated steatosis to metabolic dysfunction-associated steatohepatitis (MASH). Hepatocyte ballooning, indicative of hepato-cellular damage, and liver inflammation, with or without fibrosis, are characteristic of MASH. Evidence shows that peroxisome proliferator-activated receptor β/δ (PPARβ/δ), expressed in the major liver cells (hepatocytes, Kupffer cells, cholangiocytes, and hepatic stellate cells), may help prevent the progression of MASLD by ameliorating insulin resistance, lipotoxicity, inflammation, and fibrosis. In this review, we summarize the molecular mechanisms by which PPARβ/δ attenuates the progression of MASLD and discuss future research perspectives.