The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Oxidative stress during acetaminophen hepatotoxicity: Sources, pathophysiological role and therapeutic potential
Open accessAbstract
Acetaminophen (APAP) hepatotoxicity is characterized by an extensive oxidative stress. However, its source, pathophysiological role and possible therapeutic potential if targeted, have been controversially described. Earlier studies argued for cytochrome P450-generated reactive oxygen species (ROS) during APAP metabolism, which resulted in massive lipid peroxidation and subsequent liver injury. However, subsequent studies convincingly challenged this assumption and the current paradigm suggests that mitochondria are the main source of ROS, which impair mitochondrial function and are responsible for cell signaling resulting in cell death. Although immune cells can be a source of ROS in other models, no reliable evidence exists to support a role for immune cell-derived ROS in APAP hepatotoxicity. Recent studies suggest that mitochondrial targeted antioxidants can be viable therapeutic agents against hepatotoxicity induced by APAP overdose, and re-purposing existing drugs to target oxidative stress and other concurrent signaling events can be a promising strategy to increase its potential application in patients with APAP overdose.
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Cites
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Sterile inflammation in the liver
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“…pathophysiology of cell injury is typically assumed when parameters of LPO (e.g., malondialdehyde, ethane and pentane exhalation, formation of hydroxyfatty acids, hydroxynonenal, etc.) are increased in the injured tissue, but decreased after an intervention that is thought to act as an antioxidant.”
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Cited by
Nrf2, the Master Regulator of Anti-Oxidative Responses
Vomund, S., Schäfer, A., Parnham, M., Brüne, B., & Von Knethen, A. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18122772 · Cited by 752
Reproducing human and cross-species drug toxicities using a liver-chip
Jang, K.-J., Otieno, M. A., Ronxhi, J., Lim, H.-K., Ewart, L., Kodella, K. R., Petropolis, D. B., Kulkarni, G., Rubins, J. E., Conegliano, D., et al. (2019) · Science Translational Medicine · doi:10.1126/scitranslmed.aax5516 · Cited by 511
Prenatal fever and autism risk
Hornig, M., Bresnahan, M. A., Che, X., Schultz, A. F., Ukaigwe, J. E., Eddy, M. L., Hirtz, D., Gunnes, N., Lie, K. K., Magnus, P., et al. (2018) · Molecular Psychiatry · doi:10.1038/mp.2017.119 · Cited by 222
LeFort, K. R., Rungratanawanich, W., & Song, B.-J. (2024) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-05061-7 · Cited by 202
Qin, Z., Ren, T., Zhou, H., Zhang, X., He, L., Li, Z., Zhang, X., & Yuan, L. (2022) · Angewandte Chemie International Edition · doi:10.1002/anie.202201541 · Cited by 140
Metadata
- Authors
- Du, K., Ramachandran, A., & Jaeschke, H.
- Venue
- Redox Biology
- Publisher
- Elsevier BV
- Published
- 2016-12
- Volume
- 10
- Pages
- 148-156
- ISSN
- 2213-2317 (ISSN-L)
- OpenAlex
- W2529405505
- Cited by
- 569
- References
- 12
- FWCI
- 50.35
- Type
- journal article
- Language
- en
- Open access
- gold
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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