Iron, Oxidative Stress, and Metabolic Dysfunction-Associated Steatotic Liver Disease

S Gensluckner, B Wernly (Co-author), C Datz, E Aigner* (Last author)

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

18 Citations (Web of Science)

Abstract

Excess free iron is a substrate for the formation of reactive oxygen species (ROS), thereby augmenting oxidative stress. Oxidative stress is a well-established cause of organ damage in the liver, the main site of iron storage. Ferroptosis, an iron-dependent mechanism of regulated cell death, has recently been gaining attention in the development of organ damage and the progression of liver disease. We therefore summarize the main mechanisms of iron metabolism, its close connection to oxidative stress and ferroptosis, and its particular relevance to disease mechanisms in metabolic-dysfunction-associated fatty liver disease and potential targets for therapy from a clinical perspective.

Original languageEnglish
Number of pages12
JournalAntioxidants
Volume13
Issue number2
DOIs
Publication statusPublished - 7 Feb 2024

Keywords

  • iron metabolism
  • oxidative stress
  • ferroptosis
  • MASLD
  • liver fibrosis
  • HEPATOCELLULAR-CARCINOMA
  • CELL-DEATH
  • FERROPTOSIS
  • OVERLOAD
  • ACTIVATION
  • FIBROSIS
  • DYSREGULATION
  • HOMEOSTASIS
  • INJURY
  • Oxidative stress
  • Iron metabolism
  • Ferroptosis
  • Liver fibrosis
  • Masld

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