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Iron-Induced Liver Injury: A Critical Reappraisal
Journal article   Open access   Peer reviewed

Iron-Induced Liver Injury: A Critical Reappraisal

Steven A. Bloomer and Kyle E. Brown
International journal of molecular sciences, Vol.20(9), p.2132
05/01/2019
DOI: 10.3390/ijms20092132
PMCID: PMC6539962
PMID: 31052166
url
https://doi.org/10.3390/ijms20092132View
Published (Version of record) Open Access

Abstract

Iron is implicated in the pathogenesis of a number of human liver diseases. Hereditary hemochromatosis is the classical example of a liver disease caused by iron, but iron is commonly believed to contribute to the progression of other forms of chronic liver disease such as hepatitis C infection and nonalcoholic fatty liver disease. In this review, we present data from cell culture experiments, animal models, and clinical studies that address the hepatotoxicity of iron. These data demonstrate that iron overload is only weakly fibrogenic in animal models and rarely causes serious liver damage in humans, calling into question the concept that iron overload is an important cause of hepatotoxicity. In situations where iron is pathogenic, iron-induced liver damage may be potentiated by coexisting inflammation, with the resulting hepatocyte necrosis an important factor driving the fibrogenic response. Based on the foregoing evidence that iron is less hepatotoxic than is generally assumed, claims that assign a causal role to iron in liver injury in either animal models or human liver disease should be carefully evaluated.
 Biochemistry & Molecular Biology Chemistry Chemistry, Multidisciplinary Life Sciences & Biomedicine Physical Sciences Science & Technology

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