NADPH Oxidases and Chronic Inflammation-Associated Cancers
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 2589
Special Issue Editor
Interests: cancer; cytokine-mediated enzymatic up-regulation; hydrogen peroxide; inflammation; NADPH oxidases; oxidative stress; reactive oxygen species; superoxide
Special Issue Information
Dear Colleagues,
You are cordially invited to submit original research articles and reviews for a new Special Issue entitled "NADPH Oxidases and Chronic Inflammation-Associated Cancers".
Chronic inflammation is a pathological condition characterized by a continued active inflammation response and tissue destruction. During chronic inflammation, a wide array of intracellular signaling pathways, comprising cell surface receptors, kinases, and transcription factors, are often dysregulated, leading to abnormal expression of pro-inflammatory genes involved in malignant transformation. Currently, epidemiological data indicate that over 25% of all cancers are related to chronic infection and other types of unresolved inflammation. Mounting evidence supports the hypothesis that chronic inflammation is an important risk factor for the development of cancer, including the observation that prolonged use of non-steroidal anti-inflammatory drugs (NSAIDs) demonstrates protective action against the development of colon adenomas, and breast, prostate, and lung cancers.
Oxidative stress plays a critical role in modulating the immune response to inflammatory stimuli. Recent evidence suggests that one source of ROS that accompanies acute and chronic inflammation in many organs is one or more members of the NADPH oxidase (NOX) family. NOX membrane proteins (NOX1-5, (Dual oxidase) DUOX1-2) catalyze isoform-specific superoxide or hydrogen peroxide generation in non-phagocytic cells, including vascular endothelium and tumor cells. There is a growing body of evidence demonstrating that one major effect of inflammation-induced cytokine secretion is the up-regulation of NOX homologues, contributing to the development of an oxidative microenvironment. This site- and tumor tissue-specific ROS formation influences tissue injury, DNA damage, and activation of a DNA repair response; therefore, efforts to prevent NOX up-regulation or to interfere with NOX function in chronic inflammatory states may be one important approach to preventing oxidative stress-related carcinogenesis.
This Special Issue aims to provide a forum collection of the latest in vitro and in vivo studies on the role of NAPDH oxidase-produced ROS in the initiation and progression of cancers related to chronic inflammation.
We look forward to your contribution.
Dr. Jennifer L. Meitzler
Guest Editor
Manuscript Submission Information
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Keywords
- NADPH oxidases
- inflammation
- cancer
- oxidative stress
- reactive oxygen species