Crosstalk between mitochondria and NADPH oxidases
By S. Dikalov. Free Radical Biology & Medicine, 2011
771 citations recorded by the source corpus.
Reactive oxygen species (ROS) play an important role in physiological and pathological processes. In recent years, a feed-forward regulation of the ROS sources has been reported. The interaction between main cellular sources of ROS, such as mitochondria and NADPH oxidases, however, remain obscure. This work summarizes the latest findings on the role of crosstalk between mitochondria and NADPH oxidases in pathophysiological processes. Mitochondria have the highest levels of antioxidants in the cell and play an important role in the maintenance of cellular redox status, thereby acting as an ROS and redox sink and limiting NADPH oxidase activity. Mitochondria, however, are not only a target for ROS produced by NADPH oxidase but also a significant source of ROS, which under certain condition may stimulate NADPH oxidases. This crosstalk between mitochondria and NADPH oxidases, therefore, may represent a feed-forward vicious cycle of ROS production which can be pharmacologically targeted under conditions of oxidative stress. It has been demonstrated that mitochondria-targeted antioxidants break this vicious cycle, inhibiting ROS production by mitochondria and reducing NADPH oxidase activity. This may provide a novel strategy for treatment of many pathological conditions including aging, atherosclerosis, diabetes, hypertension and degenerative neurological disorders in which mitochondrial oxidative stress seems to play a role. It is conceivable that the use of mitochondria-targeted treatments would be effective in these conditions.
Subfields: Immunology, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/415b052dea53d1b5b16eab7cbbc8b469005cc9ad
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Citations in the corpus
- Oxidative Stress in Obesity: A Critical Component in Human Diseases (2014, neutral): “NADPH oxidases [22].”
- Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. (2014, background): “was not found in mitochondria, and furthermore, that the specific activity of Nox in mitochondria is not measurable (111).”
- Reactive Oxygen Species in Inflammation and Tissue Injury (2014, positive): “A dysregulation in this relationship may drive the vicious feed-forward cycle of ROS accumulation that can enhance inflammatory response in different diseases (96, 380).”
- Reciprocal regulation of TGF-β and reactive oxygen species: A perverse cycle for fibrosis (2015, positive): “Emerging evidence suggests that there is crosstalk between mitochondria and NADPH oxidases: mitochondria-derived ROS contribute to the increase in NOX expression in response to TGF-β whereas NOX-generated ROS cause mitochondria dysfunction and increase mitochondrial ROS production [121 – 124].”