The DOI matches its Crossref record; 106 of the 106 references it cites were found in a registry or an index.
Ferroptosis in liver disease: new insights into disease mechanisms
Open accessAbstract
Characterized by excessive iron accumulation and lipid peroxidation, ferroptosis is a novel form of iron-dependent cell death, which is morphologically, genetically, and biochemically distinct from other well-known cell death. In recent years, ferroptosis has been quickly gaining attention in the field of liver diseases, as the liver is predisposed to oxidative injury and generally, excessive iron accumulation is a primary characteristic of most major liver diseases. In the current review, we first delineate three cellular defense mechanisms against ferroptosis (GPx4 in the mitochondria and cytosol, FSP1 on plasma membrane, and DHODH in mitochondria), along with four canonical modulators of ferroptosis (system Xc−, nuclear factor erythroid 2-related factor 2, p53, and GTP cyclohydrolase-1). Next, we review recent progress of ferroptosis studies delineating molecular mechanisms underlying the pathophysiology of several common liver diseases including ischemia/reperfusion-related injury (IRI), nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), hemochromatosis (HH), drug-induced liver injury (DILI), and hepatocellular carcinoma (HCC). Furthermore, we also highlight both challenges and promises that emerged from recent studies that should be addressed and pursued in future investigations before ferroptosis regulation could be adopted as an effective therapeutic target in clinical practice.
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Cites
Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death
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Regulation of Ferroptotic Cancer Cell Death by GPX4
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Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease
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Self-citationGlobal burden of NAFLD and NASH: trends, predictions, risk factors and prevention
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ACSL4 dictates ferroptosis sensitivity by shaping cellular lipid composition
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Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice
Friedmann Angeli, J. P., Schneider, M., Proneth, B., Tyurina, Y. Y., Tyurin, V. A., Hammond, V. J., Herbach, N., Aichler, M., Walch, A., Eggenhofer, E., et al. (2014) · Nature Cell Biology · doi:10.1038/ncb3064 · Cited by 3,732
The CoQ oxidoreductase FSP1 acts parallel to GPX4 to inhibit ferroptosis
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Ferroptosis as a p53-mediated activity during tumour suppression
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FSP1 is a glutathione-independent ferroptosis suppressor
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Cited by
GPX4, ferroptosis, and diseases
Zhang, W., Liu, Y., Liao, Y., Zhu, C., & Zou, Z. (2024) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2024.116512 · Cited by 426
Polyunsaturated Fatty Acids Drive Lipid Peroxidation during Ferroptosis
Mortensen, M. S., Ruiz, J., & Watts, J. L. (2023) · Cells · doi:10.3390/cells12050804 · Cited by 312
Recent Advances in Understanding of Pathogenesis of Alcohol-Associated Liver Disease
Wu, X., Fan, X., Miyata, T., Kim, A., Cajigas-Du Ross, C. K., Ray, S., Huang, E., Taiwo, M., Arya, R., Wu, J., et al. (2023) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathmechdis-031521-030435 · Cited by 289
Self-citationMitochondrial Management of Reactive Oxygen Species
Napolitano, G., Fasciolo, G., & Venditti, P. (2021) · Antioxidants · doi:10.3390/antiox10111824 · Cited by 281
Metadata
- Authors
- Wu, J., Wang, Y., Jiang, R., Xue, R., Yin, X., Wu, M., & Meng, Q.
- Venue
- Cell Death Discovery
- Published
- 2021-10-05
- Volume
- 7
- Issue
- 1
- Pages
- 276-276
- ISSN
- 2058-7716 (ISSN-L)
- OpenAlex
- W3202493769
- Cited by
- 281
- References
- 106
- FWCI
- 24.54
- Type
- journal article
- Language
- en
- Open access
- gold
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