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The Role of NRF2 in Health and Disease
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The Role of NRF2 in Health and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 3692

Special Issue Editors

Dr. Daniela Impellizzeri

E-Mail Website
Guest Editor
Department of Chemical biological, pharmaceutical and environmental sciences, Università degli Studi di Messina, 98166 Messina, Italy
Interests: inflammation; oxidative stress; biochemistry; pharmacology; molecular biology
Special Issues, Collections and Topics in MDPI journals
Dr. Ramona D'Amico

E-Mail Website
Guest Editor
Department of Chemical Biological, Pharmaceutical and Environmental Sciences, Università degli Studi di Messina, 98166 Messina, Italy
Interests: biomarkers; molecular pathways; oxidative stress; inflammation; natural compound; clinical and pre-clinical studies
Special Issues, Collections and Topics in MDPI journals
Dr. Rosalba Siracusa

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Interests: clinical biochemistry; inflammation; oxidative stress; neurodegeneration; natural compounds
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a major transcription factor involved in redox homeostasis and in the response induced by oxidative injury. It plays a major role in the dynamic regulation of a network of antioxidant and cytoprotective genes through binding to and activating the expression of promoters containing the antioxidant response element (ARE). Nrf2 activity is regulated by many mechanisms, suggesting that tight control is necessary for normal cell function, and both the hypoactivation and hyperactivation of Nrf-2 could play a role in various aspects of inflammatory diseases. Multiple classes of chemical inducers are known to elevate endogenous antioxidants by activating Nrf2. This Special Issue will focus on the role of NRF-2 in health or disease conditions and on the targeted activation of the Nrf-2 pathway, which could be a useful avenue in developing new therapeutics.

The Special Issue will feature original articles on in vivo and in vitro studies and reviews.

Dr. Daniela Impellizzeri
Dr. Ramona D'Amico
Dr. Rosalba Siracusa
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • disease
  • inflammation
  • oxidative stress
  • therapeutics
  • animal models studies
  • in vitro studies

Published Papers (3 papers)

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Research

25 pages, 21251 KiB  
Article
KEAP1-Mutant Lung Cancers Weaken Anti-Tumor Immunity and Promote an M2-like Macrophage Phenotype
by Christopher J. Occhiuto and Karen T. Liby
Int. J. Mol. Sci. 2024, 25(6), 3510; https://doi.org/10.3390/ijms25063510 - 20 Mar 2024
Viewed by 629
Abstract
Considerable advances have been made in lung cancer therapies, but there is still an unmet clinical need to improve survival for lung cancer patients. Immunotherapies have improved survival, although only 20–30% of patients respond to these treatments. Interestingly, cancers with mutations in Kelch-like [...] Read more.
Considerable advances have been made in lung cancer therapies, but there is still an unmet clinical need to improve survival for lung cancer patients. Immunotherapies have improved survival, although only 20–30% of patients respond to these treatments. Interestingly, cancers with mutations in Kelch-like ECH-associated protein 1 (KEAP1), the negative regulator of the nuclear factor erythroid 2-related factor 2 (NRF2) transcription factor, are resistant to immune checkpoint inhibition and correlate with decreased lymphoid cell infiltration. NRF2 is known for promoting an anti-inflammatory phenotype when activated in immune cells, but the study of NRF2 activation in cancer cells has not been adequately assessed. The objective of this study was to determine how lung cancer cells with constitutive NRF2 activity interact with the immune microenvironment to promote cancer progression. To assess, we generated CRISPR-edited mouse lung cancer cell lines by knocking out the KEAP1 or NFE2L2 genes and utilized a publicly available single-cell dataset through the Gene Expression Omnibus to investigate tumor/immune cell interactions. We show here that KEAP1-mutant cancers promote immunosuppression of the tumor microenvironment. Our data suggest KEAP1 deletion is sufficient to alter the secretion of cytokines, increase expression of immune checkpoint markers on cancer cells, and alter recruitment and differential polarization of immunosuppressive macrophages that ultimately lead to T-cell suppression. Full article
(This article belongs to the Special Issue The Role of NRF2 in Health and Disease)
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20 pages, 4351 KiB  
Article
Antioxidant Activity of a Sicilian Almond Skin Extract Using In Vitro and In Vivo Models
by Alessia Arangia, Agnese Ragno, Marika Cordaro, Ramona D’Amico, Rosalba Siracusa, Roberta Fusco, Francesca Marino Merlo, Antonella Smeriglio, Daniela Impellizzeri, Salvatore Cuzzocrea, Giuseppina Mandalari and Rosanna Di Paola
Int. J. Mol. Sci. 2023, 24(15), 12115; https://doi.org/10.3390/ijms241512115 - 28 Jul 2023
Cited by 2 | Viewed by 1217
Abstract
Almond skins are known for their antioxidative and anti-inflammatory properties, which are mainly due to the presence of polyphenols. The aim of the present study was to evaluate the antioxidant and anti-inflammatory effects of almond skin extract (ASE) obtained from the Sicilian cultivar [...] Read more.
Almond skins are known for their antioxidative and anti-inflammatory properties, which are mainly due to the presence of polyphenols. The aim of the present study was to evaluate the antioxidant and anti-inflammatory effects of almond skin extract (ASE) obtained from the Sicilian cultivar “Fascionello” and to evaluate the possible mechanisms of action using an in vitro model of human monocytic U937 cells as well as an in vivo model of carrageenan (CAR)-induced paw edema. The in vitro studies demonstrated that pretreatment with ASE inhibited the formation of ROS and apoptosis. The in vivo studies showed that ASE restored the CAR-induced tissue changes; restored the activity of endogenous antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione; and decreased neutrophil infiltration, lipid peroxidation, and the release of proinflammatory mediators. The anti-inflammatory and antioxidant effects of ASE could be associated with the inhibition of the pro-inflammatory nuclear NF-κB and the activation of the nuclear factor-erythroid 2-related factor 2 (Nrf2) antioxidant pathways. In conclusion, almond skin could reduce the levels of inflammation and oxidative stress and could be beneficial in the treatment of several disorders. Full article
(This article belongs to the Special Issue The Role of NRF2 in Health and Disease)
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27 pages, 6762 KiB  
Article
The Effect of Cerebrolysin in an Animal Model of Forebrain Ischemic-Reperfusion Injury: New Insights into the Activation of the Keap1/Nrf2/Antioxidant Signaling Pathway
by Basma H. Marghani, Shaymaa Rezk, Ahmed I. Ateya, Badriyah S. Alotaibi, Basma H. Othman, Samy M. Sayed, Mohammed Ali Alshehri, Mustafa Shukry and Mohamed M. Mansour
Int. J. Mol. Sci. 2023, 24(15), 12080; https://doi.org/10.3390/ijms241512080 - 28 Jul 2023
Cited by 1 | Viewed by 1264
Abstract
Forebrain ischemia-reperfusion (IR) injury causes neurological impairments due to decreased cerebral autoregulation, hypoperfusion, and edema in the hours to days following the restoration of spontaneous circulation. This study aimed to examine the protective and/or therapeutic effects of cerebrolysin (CBL) in managing forebrain IR [...] Read more.
Forebrain ischemia-reperfusion (IR) injury causes neurological impairments due to decreased cerebral autoregulation, hypoperfusion, and edema in the hours to days following the restoration of spontaneous circulation. This study aimed to examine the protective and/or therapeutic effects of cerebrolysin (CBL) in managing forebrain IR injury and any probable underlying mechanisms. To study the contribution of reperfusion to forebrain injury, we developed a transient dual carotid artery ligation (tDCAL/IR) mouse model. Five equal groups of six BLC57 mice were created: Group 1: control group (no surgery was performed); Group 2: sham surgery (surgery was performed without IR); Group 3: tDCAL/IR (surgery with IR via permanently ligating the left CA and temporarily closing the right CA for 30 min, followed by reperfusion for 72 h); Group 4: CBL + tDCAL/IR (CBL was given intravenously at a 60 mg/kg BW dose 30 min before IR); and Group 5: tDCAL/IR + CBL (CBL was administered i.v. at 60 mg/kg BW three hours after IR). At 72 h following IR, the mice were euthanized. CBL administration 3 h after IR improved neurological functional recovery, enhanced anti-inflammatory and antioxidant activities, alleviated apoptotic neuronal death, and inhibited reactive microglial and astrocyte activation, resulting in neuroprotection after IR injury in the tDCAL/IR + CBL mice group as compared to the other groups. Furthermore, CBL reduced the TLRs/NF-kB/cytokines while activating the Keap1/Nrf2/antioxidant signaling pathway. These results indicate that CBL may improve neurologic function in mice following IR. Full article
(This article belongs to the Special Issue The Role of NRF2 in Health and Disease)
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