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The DOI matches its Crossref record; 141 of the 141 references it cites were found in a registry or an index.

The multifaceted role of ferroptosis in liver disease

Open access
Chen, Junyi, Li, Xiaopeng, Ge, Chaodong, Min, Junxia, Wang, Fudi·2022·Cell Death & Differentiation

Abstract

Ferroptosis is an iron-dependent form of non-apoptotic cell death characterized by excessive lipid peroxidation and associated with a plethora of pathological conditions in the liver. Emerging evidence supports the notion that dysregulated metabolic pathways and impaired iron homeostasis play a role in the progression of liver disease via ferroptosis. Although the molecular mechanisms by which ferroptosis causes disease are poorly understood, several ferroptosis-associated genes and pathways have been implicated in liver disease. Here, we review the physiological role of the liver in processing nutrients, our current understanding of iron metabolism, the characteristics of ferroptosis, and the mechanisms that regulate ferroptosis. In addition, we summarize the role of ferroptosis in the pathogenesis of liver disease, including liver injury, non-alcoholic steatohepatitis, liver fibrosis, liver cirrhosis, and hepatocellular carcinoma. Finally, we discuss the therapeutic potential of targeting ferroptosis for managing liver disease.

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Metadata

Authors
Chen, J., Li, X., Ge, C., Min, J., & Wang, F.
Venue
Cell Death & Differentiation
Published
2022-01-24
Volume
29
Issue
3
Pages
467-480
ISSN
  • 1350-9047 (ISSN-L)
  • 1476-5403
OpenAlex
W4206972726
Cited by
665
References
141
FWCI
79.07
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: The multifaceted role of ferroptosis in liver disease. https://app.cochat.ai/papers/10.1038/s41418-022-00941-0
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Chen, J., Li, X., Ge, C., Min, J., & Wang, F. (2022). The multifaceted role of ferroptosis in liver disease. Cell Death & Differentiation. https://doi.org/10.1038/s41418-022-00941-0

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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