共 100 条
Iron, Oxidative Stress, and Metabolic Dysfunction-Associated Steatotic Liver Disease
被引:27
作者:

Gensluckner, Sophie
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机构:
Paracelsus Med Univ, Dept Internal Med 1, Mullner Hauptstr 48, A-5020 Salzburg, Austria
Paracelsus Med Univ, Obes Res Unit, A-5020 Salzburg, Austria Paracelsus Med Univ, Dept Internal Med 1, Mullner Hauptstr 48, A-5020 Salzburg, Austria

Wernly, Bernhard
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h-index: 0
机构:
Paracelsus Med Univ, Gen Hosp Oberndorf, Dept Med, Teaching Hosp, A-5110 Oberndorf, Austria Paracelsus Med Univ, Dept Internal Med 1, Mullner Hauptstr 48, A-5020 Salzburg, Austria

Datz, Christian
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h-index: 0
机构:
Paracelsus Med Univ, Gen Hosp Oberndorf, Dept Med, Teaching Hosp, A-5110 Oberndorf, Austria Paracelsus Med Univ, Dept Internal Med 1, Mullner Hauptstr 48, A-5020 Salzburg, Austria

Aigner, Elmar
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h-index: 0
机构:
Paracelsus Med Univ, Dept Internal Med 1, Mullner Hauptstr 48, A-5020 Salzburg, Austria
Paracelsus Med Univ, Obes Res Unit, A-5020 Salzburg, Austria Paracelsus Med Univ, Dept Internal Med 1, Mullner Hauptstr 48, A-5020 Salzburg, Austria
机构:
[1] Paracelsus Med Univ, Dept Internal Med 1, Mullner Hauptstr 48, A-5020 Salzburg, Austria
[2] Paracelsus Med Univ, Obes Res Unit, A-5020 Salzburg, Austria
[3] Paracelsus Med Univ, Gen Hosp Oberndorf, Dept Med, Teaching Hosp, A-5110 Oberndorf, Austria
关键词:
iron metabolism;
oxidative stress;
ferroptosis;
MASLD;
liver fibrosis;
HEPATOCELLULAR-CARCINOMA;
CELL-DEATH;
FERROPTOSIS;
OVERLOAD;
ACTIVATION;
FIBROSIS;
DYSREGULATION;
HOMEOSTASIS;
INJURY;
D O I:
10.3390/antiox13020208
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
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.
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