Iron-induced liver injury: A critical reappraisal

Steven Alfred Bloomer, Kyle E. Brown

Research output: Contribution to journalArticle

1 Citation (Scopus)

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.

Original languageEnglish (US)
Article number2132
JournalInternational journal of molecular sciences
Volume20
Issue number9
DOIs
StatePublished - May 1 2019

Fingerprint

liver
Liver
Iron
iron
Wounds and Injuries
Liver Diseases
animal models
Iron Overload
Animal Models
Animals
Hemochromatosis
hepatitis
damage
Hepatitis C
pathogenesis
necrosis
causes
Hepatocytes
infectious diseases
Chronic Disease

All Science Journal Classification (ASJC) codes

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

@article{7c13b002ce6a4c84b4d9ac76119d58d8,
title = "Iron-induced liver injury: A critical reappraisal",
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.",
author = "Bloomer, {Steven Alfred} and Brown, {Kyle E.}",
year = "2019",
month = "5",
day = "1",
doi = "10.3390/ijms20092132",
language = "English (US)",
volume = "20",
journal = "International Journal of Molecular Sciences",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "9",

}

Iron-induced liver injury : A critical reappraisal. / Bloomer, Steven Alfred; Brown, Kyle E.

In: International journal of molecular sciences, Vol. 20, No. 9, 2132, 01.05.2019.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Iron-induced liver injury

T2 - A critical reappraisal

AU - Bloomer, Steven Alfred

AU - Brown, Kyle E.

PY - 2019/5/1

Y1 - 2019/5/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=85065647456&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85065647456&partnerID=8YFLogxK

U2 - 10.3390/ijms20092132

DO - 10.3390/ijms20092132

M3 - Article

C2 - 31052166

AN - SCOPUS:85065647456

VL - 20

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1661-6596

IS - 9

M1 - 2132

ER -