The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Mechanisms of Liver Injury. I. TNF-α-induced liver injury: role of IKK, JNK, and ROS pathways
Abstract
TNF-α activates several intracellular pathways to regulate inflammation, cell death, and proliferation. In the liver, TNF-α is not only a mediator of hepatotoxicity but also contributes to the restoration of functional liver mass by driving hepatocyte proliferation and liver regeneration. This review summarizes recent advances in TNF-α signaling mechanisms that demonstrate how the IKK, ROS, and JNK pathways interact with each other to regulate hepatocyte apoptosis and proliferation. Activation of these pathways is causatively linked to liver injury induced by concanavalin A, TNF-α, and ischemia-reperfusion and to liver regeneration and hepatocarcinogenesis. In light of recent findings, pharmacological inhibitors of JNK and IKK and antioxidants may be promising new tools for the treatment of hepatitis, ischemia-reperfusion injury, and hepatocellular carcinoma.
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Cites
Missing Pieces in the NF-κB Puzzle
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Induction of gadd45β by NF-κB downregulates pro-apoptotic JNK signalling
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IKKβ Is Required for Prevention of Apoptosis Mediated by Cell-Bound but Not by Circulating TNFα
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Reparative inflammation takes charge of tissue regeneration
Karin, M., & Clevers, H. (2016) · Nature · doi:10.1038/nature17039 · Cited by 767
Festjens, N., Vanden Berghe, T., & Vandenabeele, P. (2006) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/j.bbabio.2006.06.014 · Cited by 710
Apoptosis and necroptosis in the liver: a matter of life and death
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Self-citationMolecular mechanisms of lipotoxicity and glucotoxicity in nonalcoholic fatty liver disease
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Control of cccDNA function in hepatitis B virus infection
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Metadata
- Authors
- Schwabe, R. F., & Brenner, D. A.
- Venue
- American Journal of Physiology-Gastrointestinal and Liver Physiology
- Publisher
- American Physiological Society
- Published
- 2006-04
- Volume
- 290
- Issue
- 4
- Pages
- G583-G589
- ISSN
- 0193-1857 (ISSN-L)
- 1522-1547
- OpenAlex
- W2155772701
- Cited by
- 685
- References
- 5
- FWCI
- 27.28
- Type
- journal article
- Language
- en
- Open access
- closed
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