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Antioxidants
Special Issues
Oxidative Stress and Nrf2-Mediated Cellular Inflammation
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Oxidative Stress and Nrf2-Mediated Cellular Inflammation

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: 30 July 2024 | Viewed by 809

Special Issue Editors

Prof. Dr. Amelia Cataldi

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Guest Editor
Department of Pharmacy, University “G. d’Annunzio” Chieti-Pescara, Via dei Vestini 31, 66100 Chieti, Italy
Interests: mesenchymal stem cell differentiation; biomaterials; tissue regeneration; hyaluronic acid; histology
Special Issues, Collections and Topics in MDPI journals
Dr. Marialucia Gallorini

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Guest Editor
Department of Pharmacy, University “G. d’Annunzio” Chieti-Pescara, Via dei Vestini 31, 66100 Chieti, Italy
Interests: inflammation; hyaluronic acid; biomaterials; oxidative stress; tendons
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nuclear factor erythroid 2‐related factor 2 (NRF2) is a master transcriptional regulator of genes whose products defend our cells from toxic and oxidative insults. NRF2 can influence several cellular functions as it is located at the intersection of crucial signaling pathways in the maintenance of the intracellular redox balance, including cellular metabolism, proteostasis, mitochondrial function and inflammation. Oxidative stress boosts NRF2 activation and links NRF2 with the activation of inflammasomes. Failure in NRF2 activation or its degradation leads to increased inflammation and the secretion of pro-inflammatory cytokines. Exaggerated inflammation negatively evolves into apoptosis/pyroptosis.

In recent decades, a plethora of literature has focused on the investigation of NRF2 modulation for therapeutic purposes, which requires accurate knowledge of the cell context and the specific timeframe both of NRF2 activation and inhibition. This Special Issue offers an overview on the most recent findings regarding the involvement of NRF2 in the modulation of cellular inflammation at a molecular level.

Prof. Dr. Amelia Cataldi
Dr. Marialucia Gallorini
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

  • Nrf2
  • oxidative stress
  • cell signaling
  • inflammation

Published Papers (1 paper)

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Research

18 pages, 3912 KiB  
Article
NLRX1 Inhibits LPS-Induced Microglial Death via Inducing p62-Dependent HO-1 Expression, Inhibiting MLKL and Activating PARP-1
by Yu-Ling Huang, Duen-Yi Huang, Vladlen Klochkov, Chi-Ming Chan, Yuan-Shen Chen and Wan-Wan Lin
Antioxidants 2024, 13(4), 481; https://doi.org/10.3390/antiox13040481 - 17 Apr 2024
Viewed by 586
Abstract
The activation of microglia and the production of cytokines are key factors contributing to progressive neurodegeneration. Despite the well-recognized neuronal programmed cell death regulated by microglial activation, the death of microglia themselves is less investigated. Nucleotide-binding oligomerization domain, leucine-rich repeat-containing X1 (NLRX1) functions [...] Read more.
The activation of microglia and the production of cytokines are key factors contributing to progressive neurodegeneration. Despite the well-recognized neuronal programmed cell death regulated by microglial activation, the death of microglia themselves is less investigated. Nucleotide-binding oligomerization domain, leucine-rich repeat-containing X1 (NLRX1) functions as a scaffolding protein and is involved in various central nervous system diseases. In this study, we used the SM826 microglial cells to understand the role of NLRX1 in lipopolysaccharide (LPS)-induced cell death. We found LPS-induced cell death is blocked by necrostatin-1 and zVAD. Meanwhile, LPS can activate poly (ADP-ribose) polymerase-1 (PARP-1) to reduce DNA damage and induce heme oxygenase (HO)-1 expression to counteract cell death. NLRX1 silencing and PARP-1 inhibition by olaparib enhance LPS-induced SM826 microglial cell death in an additive manner. Less PARylation and higher DNA damage are observed in NLRX1-silencing cells. Moreover, LPS-induced HO-1 gene and protein expression through the p62-Keap1-Nrf2 axis are attenuated by NLRX1 silencing. In addition, the Nrf2-mediated positive feedback regulation of p62 is accordingly reduced by NLRX1 silencing. Of note, NLRX1 silencing does not affect LPS-induced cellular reactive oxygen species (ROS) production but increases mixed lineage kinase domain-like pseudokinase (MLKL) activation and cell necroptosis. In addition, NLRX1 silencing blocks bafilomycin A1-induced PARP-1 activation. Taken together, for the first time, we demonstrate the role of NLRX1 in protecting microglia from LPS-induced cell death. The underlying protective mechanisms of NLRX1 include upregulating LPS-induced HO-1 expression via Nrf2-dependent p62 expression and downstream Keap1-Nrf2 axis, mediating PARP-1 activation for DNA repair via ROS- and autophagy-independent pathway, and reducing MLKL activation. Full article
(This article belongs to the Special Issue Oxidative Stress and Nrf2-Mediated Cellular Inflammation)
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