Format

Send to

Choose Destination
Int J Biochem Cell Biol. 2016 Dec;81(Pt B):281-293. doi: 10.1016/j.biocel.2016.06.015. Epub 2016 Jun 29.

Mitochondrial reactive oxygen species and inflammation: Molecular mechanisms, diseases and promising therapies.

Author information

1
Dept. of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy.
2
Dept. of Morphology, Surgery and Experimental Medicine, Section of Human Anatomy and Histology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy.
3
Dept. of Biochemistry, Nencki Institute of Experimental Biology, Warsaw, Poland. Electronic address: m.wieckowski@nencki.gov.pl.
4
Dept. of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy. Electronic address: pnp@unife.it.

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.

KEYWORDS:

Inflammasome; Inflammation-related diseases; Inflammatory response; Mitochondrial dysfunction; ROS

PMID:
27373679
DOI:
10.1016/j.biocel.2016.06.015
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center