# Unveiling the Crucial Nexus: Mitochondrial Quality Control as a Central Driver in Metabolic Dysfunction‐Associated Steatotic Liver Disease Pathogenesis

## TL;DR

This paper explores how mitochondrial quality control issues contribute to liver disease and suggests new treatment approaches.

## Contribution

The study highlights novel therapeutic strategies targeting mitochondrial dysfunction in MASLD.

## Key findings

- Impaired mitochondrial quality control drives MASLD through mechanisms like reduced mitophagy and increased fission.
- Pathological processes like hepatocyte apoptosis and ferroptosis are linked to MQC dysfunction.
- Potential therapies include autophagy enhancers and ferroptosis inhibitors.

## Abstract

Mitochondrial quality control (MQC) impairment plays a central role in driving the pathogenesis of metabolism‐associated steatotic liver disease (MASLD). Specifically, this is manifested as reduced mitophagy; increased mitochondrial fission and decreased fusion; and impaired mitochondrial biogenesis. Key pathological mechanisms of MASLD, such as hepatocyte apoptosis, pyroptosis, and ferroptosis, are activated under the influence of factors including free fatty acids (FFAs), oxidative stress, NLRP3 inflammasome activation, and gut microbiota imbalance. Meanwhile, the letter also lists novel potential therapeutic strategies targeting these pathways, including autophagy enhancers, mitochondrial dynamics regulators, biogenesis promoters, and ferroptosis inhibitors.