Mitochondrial dysfunction as a trigger of innate immune responses and inflammation
Toxicology, ISSN: 0300-483X, Vol: 391, Page: 54-63
2017
- 152Citations
- 204Captures
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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
- Citations152
- Citation Indexes152
- 152
- CrossRef123
- Captures204
- Readers204
- 204
Article Description
A growing literature indicates that mitochondria are key participants in innate immune pathways, functioning as both signaling platforms and contributing to effector responses. In addition to regulating antiviral signaling and antibacterial immunity, mitochondria are also important drivers of inflammation caused by sterile injury. Much research on mitochondrial control of immunity now centers on understanding how mitochondrial constituents released during cellular damage simulate the innate immune system. When mitochondrial integrity is compromised, mitochondrial damage-associated molecular patterns engage pattern recognition receptors, trigger inflammation, and promote pathology in an expanding list of diseases. Here, I review the emerging knowledge of mitochondrial dysfunction in innate immune responses and discuss how environmental exposures may induce mitochondrial damage to potentiate inflammation and human disease.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0300483X17302159; http://dx.doi.org/10.1016/j.tox.2017.07.016; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85026741885&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/28765055; https://linkinghub.elsevier.com/retrieve/pii/S0300483X17302159; https://dx.doi.org/10.1016/j.tox.2017.07.016
Elsevier BV
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