| Literature DB >> 27373679 |
Alessandro Rimessi1, Maurizio Previati2, Federica Nigro1, Mariusz R Wieckowski3, Paolo Pinton4.
Abstract
Over the last few decades, many different groups have been engaged in studies of new roles for mitochondria, particularly the coupling of alterations in the redox pathway with the inflammatory responses involved in different diseases, including Alzheimer's disease, Parkinson's disease, atherosclerosis, cerebral cavernous malformations, cystic fibrosis and cancer. Mitochondrial dysfunction is important in these pathological conditions, suggesting a pivotal role for mitochondria in the coordination of pro-inflammatory signaling from the cytosol and signaling from other subcellular organelles. In this regard, mitochondrial reactive oxygen species are emerging as perfect liaisons that can trigger the assembly and successive activation of large caspase-1- activating complexes known as inflammasomes. This review offers a glimpse into the mechanisms by which inflammasomes are activated by mitochondrial mechanisms, including reactive oxygen species production and mitochondrial Ca2+ uptake, and the roles they can play in several inflammatory pathologies.Entities:
Keywords: Inflammasome; Inflammation-related diseases; Inflammatory response; Mitochondrial dysfunction; ROS
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Year: 2016 PMID: 27373679 DOI: 10.1016/j.biocel.2016.06.015
Source DB: PubMed Journal: Int J Biochem Cell Biol ISSN: 1357-2725 Impact factor: 5.085