Death receptor interactions with the mitochondrial cell death pathway during immune cell-, drug- and toxin-induced liver damage
Frontiers in Cell and Developmental Biology, ISSN: 2296-634X, Vol: 7, Issue: APR, Page: 72
2019
- 8Citations
- 19Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations8
- Citation Indexes8
- CrossRef5
- Captures19
- Readers19
- 19
Article Description
Due to its extensive vascularization and physiological function as a filter and storage organ, the liver is constantly exposed to infectious and tumorigenic threat, as well as damaging actions of xenobiotics. Detoxification reactions are essential for the excretion of harmful substances, but harbor also the risk of "side effects" leading to dangerous metabolites of otherwise harmless substances, a well known effect during paracetamol overdose. These drugs can have detrimental effects, which often involves the induction of sterile inflammation and activation of the immune system. Therefore, the role of certain immune cells and their effector molecules in the regulation of drug-induced liver damage are of special interest. Hepatocytes are type II cells, and death receptor-induced cell death requires amplification via the mitochondrial pathway. However, this important role of the mitochondria and associated cell death-regulating signaling complexes appears to be not restricted to death receptor signaling, but to extend to drug-induced activation of mitochondrial cell death pathways. We here discuss the role of members of the Tumor Necrosis Factor family, with a focus on TRAIL, and their interactions with the Bcl-2 family in the crosstalk between the extrinsic and intrinsic cell death pathway during xenobiotic-induced liver damage.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85065119538&origin=inward; http://dx.doi.org/10.3389/fcell.2019.00072; http://www.ncbi.nlm.nih.gov/pubmed/31069226; https://www.frontiersin.org/article/10.3389/fcell.2019.00072/full; https://dx.doi.org/10.3389/fcell.2019.00072; https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2019.00072/full
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