Journal
CLINICAL & TRANSLATIONAL IMMUNOLOGY
Volume 9, Issue 2, Pages -Publisher
WILEY
DOI: 10.1002/cti2.1109
Keywords
infection; inflammasome; mitochondria; NLRP3; ROS
Categories
Funding
- National Health and Medical Research Council of Australia [1141131]
- Australian Research Council [DP160102702]
- Australian Government Research Training Program Scholarship
- Yulgilbar Alzheimer's Research Program PhD Top-up Award from the Yulgilbar Foundation
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The nod-like receptor protein 3 (NLRP3) inflammasome drives inflammation in response to mitochondrial dysfunction. As metabolic powerhouses with prokaryotic ancestry, mitochondria are a cache for danger-associated molecular patterns and pathogen-associated molecular pattern-like molecules that elicit potent innate immune responses. Persistent mitochondrial damage caused by infection, or genetic or environmental factors, can lead to inappropriate or sustained inflammasome signalling. Here, we review the features of mitochondria that drive inflammatory signalling, with a particular focus on mitochondrial activation of the NLRP3 inflammasome. Given that mitochondrial network dynamics, metabolic activity and redox state are all intricately linked to each other and to NLRP3 inflammasome activity, we highlight the importance of a holistic approach to investigations of NLRP3 activation by dysfunctional mitochondria.
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