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Related Experiment Video

Updated: Jan 5, 2026

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Mitochondrial Dysfunction in the Transition from NASH to HCC.

Mélissa Léveillé1,2, Jennifer L Estall3,4,5

  • 1Institut de Recherches Cliniques de Montréal (IRCM), Montreal, Quebec, QC H2W 1R7, Canada. Melissa.Leveille@ircm.qc.ca.

Metabolites
|October 19, 2019
PubMed
Summary

Mitochondrial dysfunction plays a key role in chronic liver diseases like non-alcoholic steatohepatitis (NASH) and liver cancer (HCC). Targeting mitochondria may offer new treatments for these conditions.

Keywords:
HCCNAFLDNASHlivermetabolismmitochondria

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Area of Science:

  • Hepatology
  • Mitochondrial Biology
  • Oncology

Background:

  • The liver's adaptation to energy demands can be compromised by harmful environmental factors, leading to chronic liver diseases.
  • Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) can progress to hepatocellular carcinoma (HCC).
  • The complex pathogenesis of these diseases is not fully understood.

Purpose of the Study:

  • To review the contribution of mitochondrial dysfunction to NASH-related HCC.
  • To explore therapeutic strategies targeting mitochondria for NASH and HCC.

Main Methods:

  • Literature review focusing on mitochondrial function in liver disease.
  • Analysis of emerging evidence linking mitochondrial alterations to disease progression.

Main Results:

  • Mitochondrial dysfunction impacts hepatocyte bioenergetics, reactive oxygen species (ROS) homeostasis, endoplasmic reticulum (ER) stress, inflammation, and cell death.
  • These cellular dysfunctions are implicated in the development of NASH and HCC.

Conclusions:

  • Altered mitochondrial function is a significant factor in NASH-related HCC.
  • Mitochondria-targeted agents represent a promising therapeutic avenue for these liver conditions.