Roles of NADPH Oxidase in Modulation of Signal Transduction and Cellular Metabolism—2nd Edition
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Antioxidant Enzyme Systems".
Deadline for manuscript submissions: 25 November 2024 | Viewed by 87
Special Issue Editors
Interests: redox signaling; NOX; GPCRs; TKRs; cellular metabolism
Special Issues, Collections and Topics in MDPI journals
Interests: signal transduction; ROS; formyl peptide receptors; NADPH oxidase; TKR-transactivation
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
We invite you to submit your latest valuable research outcomes for publication in the Second Volume of the Special Issue entitled "Roles of NADPH Oxidase in Modulation of Signal Transduction and Cellular Metabolism" for the Antioxidants journal (MDPI).
This Special Issue will focus on the emerging role of the NOX family of NADPH oxidases in the regulation of cell metabolism and redox signaling. The NOX family includes seven isoforms with different activation mechanisms, widely expressed in several tissues. The main role of these enzymes is to produce reactive oxygen species (ROS) that can act as second messengers, modulating many biological functions and cellular processes. In particular, a significant correlation of NOX-mediated oxidative stress with redox signaling and cellular metabolism has been observed in several pathological and physiological conditions. Therefore, we encourage you to contribute to this Special Issue with research or review articles, collecting data from both in vitro and in vivo to disclose the functions and role of NADPH oxidase family members in different cellular systems and their contributions to pathological and physiological conditions.
The following topics may be included in this Special Issue: NOX-dependent diseases; aging; signal transduction; cellular metabolism; metabolic reprogramming; tumor microenvironment; Warburg effect; lipid peroxidation; ferroptosis; receptor transactivation; kinase and phosphatase activation; NOX subunits; transcription; angiogenesis; cell proliferation; cell death and apoptosis; stress response; immunoregulation; inflammation; chronic granulomatous disease; NOX activators and inhibitors.
Research or review articles collecting data from both in vitro and in vivo investigations are welcome.
Prof. Rosario Ammendola
Dr. Fabio Cattaneo
Guest Editors
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
Keywords
- redox signaling
- inflammation
- NADPH oxidase
- ROS
- cell metabolism
- redox-state
- Warburg effect
- metabolic reprogramming
- tumor microenvironment
- cell proliferation
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