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Pharmacological Modulation of Oxidative Stress
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Pharmacological Modulation of Oxidative Stress

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

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 5982

Special Issue Editor

Prof. Dr. Luciano Saso

grade E-Mail Website
Guest Editor
Faculty of Pharmacy and Medicine, Sapienza University of Rome, 00185 Rome, Italy
Interests: pharmacology; therapeutic modulators of oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress has shown to play an etiopathogenetic role in a variety of conditions, including cardiovascular diseases, neurodegenerative diseases, epilepsy, and cancer. In the last two decades the role of antioxidants has been significantly redefined. The hypothesis that “classical antioxidants” (radical scavengers) could always be beneficial for human health has been questioned by several epidemiological and clinical studies. Considering these pitfalls, more favourable approach would be to target the oxidative stress induced signalling pathways involved in disease etiology or regulation of metabolic enzymes and efflux transporters. Oxidative stress activates cascade of downstream proteins and transcription factors including protein kinase cascade, NRF2, NF-KB, AP1 etc. Hence, understanding these pathways can provide potential therapeutic targets to manage pathologies accompanying oxidative stress. In this Special Issue, we aim at collecting papers on the main pharmacological aspects of oxidative stress, with special attention to the modulation Nrf2, and in particular to the beneficial effects of the pro-oxidant activity of inhibitors of Nrf2 in cancer.

Prof. Dr. Luciano Saso
Guest Editor

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

  • pharmacology
  • modulation of oxidative stress
  • NRF2
  • antioxidants
  • prooxidants

Published Papers (5 papers)

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Editorial

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3 pages, 198 KiB  
Editorial
Pharmacological Modulation of Oxidative Stress
by Sarmistha Saha and Luciano Saso
Int. J. Mol. Sci. 2023, 24(19), 14455; https://doi.org/10.3390/ijms241914455 - 22 Sep 2023
Cited by 1 | Viewed by 552
Abstract
An imbalance between the formation of reactive oxygen species (ROS) and the reaction of antioxidant proteins is referred to as oxidative stress [...] Full article
(This article belongs to the Special Issue Pharmacological Modulation of Oxidative Stress)

Research

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15 pages, 2771 KiB  
Article
Sex-Dependent Differences in the Ischemia/Reperfusion-Induced Expression of AMPA Receptors
by Lindsay M. Achzet and Darrell A. Jackson
Int. J. Mol. Sci. 2024, 25(4), 2231; https://doi.org/10.3390/ijms25042231 - 13 Feb 2024
Viewed by 503
Abstract
Following ischemia/reperfusion, AMPA receptors (AMPARs) mediate pathologic delayed neuronal death through sustained expression of calcium-permeable AMPARs, leading to excitotoxicity. Preventing the surface removal of GluA2-containing AMPARs may yield new therapeutic targets for the treatment of ischemia/reperfusion. This study utilized acute organotypic hippocampal slices [...] Read more.
Following ischemia/reperfusion, AMPA receptors (AMPARs) mediate pathologic delayed neuronal death through sustained expression of calcium-permeable AMPARs, leading to excitotoxicity. Preventing the surface removal of GluA2-containing AMPARs may yield new therapeutic targets for the treatment of ischemia/reperfusion. This study utilized acute organotypic hippocampal slices from aged male and female Sprague Dawley rats and subjected them to oxygen-glucose deprivation/reperfusion (OGD/R) to examine the mechanisms underlying the internalization and degradation of GluA2-containing AMPARs. We determined the effect of OGD/R on AMPAR subunits at the protein and mRNA transcript levels utilizing Western blot and RT-qPCR, respectively. Hippocampal slices from male and female rats responded to OGD/R in a paradoxical manner with respect to AMPARs. GluA1 and GluA2 AMPAR subunits were degraded following OGD/R in male rats but were increased in female rats. There was a rapid decrease in GRIA1 (GluA1) and GRIA2 (GluA2) mRNA levels in the male hippocampus following ischemic insult, but this was not observed in females. These data indicate a sex-dependent difference in how AMPARs in the hippocampus respond to ischemic insult, and may help explain, in part, why premenopausal women have a lower incidence/severity of ischemic stroke compared with men of the same age. Full article
(This article belongs to the Special Issue Pharmacological Modulation of Oxidative Stress)
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19 pages, 4536 KiB  
Article
Vasculoprotective Potential of Baicalein in Angiotensin II-Infused Abdominal Aortic Aneurysms through Inhibiting Inflammation and Oxidative Stress
by Erna Sulistyowati, Shang-En Huang, Tsung-Lin Cheng, Yu-Ying Chao, Chia-Yang Li, Ching-Wen Chang, Meng-Xuan Lin, Ming-Chung Lin and Jwu-Lai Yeh
Int. J. Mol. Sci. 2023, 24(21), 16004; https://doi.org/10.3390/ijms242116004 - 06 Nov 2023
Cited by 1 | Viewed by 1237
Abstract
Aortic wall inflammation, abnormal oxidative stress and progressive degradation of extracellular matrix proteins are the main characteristics of abdominal aortic aneurysms (AAAs). The nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome dysregulation plays a crucial role in aortic damage and [...] Read more.
Aortic wall inflammation, abnormal oxidative stress and progressive degradation of extracellular matrix proteins are the main characteristics of abdominal aortic aneurysms (AAAs). The nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome dysregulation plays a crucial role in aortic damage and disease progression. The first aim of this study was to examine the effect of baicalein (5,6,7-trihydroxy-2-phenyl-4H-1-benzopyran-4-one) on AAA formation in apolipoprotein E-deficient (ApoE−/−) mice. The second aim was to define whether baicalein attenuates aberrant vascular smooth muscle cell (VSMC) proliferation and inflammation in VSMC culture. For male ApoE−/− mice, a clinically relevant AAA model was randomly divided into four groups: saline infusion, baicalein intraperitoneal injection, Angiotensin II (Ang II) infusion and Ang II + baicalein. Twenty-seven days of treatment with baicalein markedly decreased Ang II-infused AAA incidence and aortic diameter, reduced collagen-fiber formation, preserved elastic structure and density and prevented smooth muscle cell contractile protein degradation. Baicalein inhibited rat VSMC proliferation and migration following the stimulation of VSMC cultures with Ang II while blocking the Ang II-inducible cell cycle progression from G0/G1 to the S phase in the synchronized cells. Cal-520 AM staining showed that baicalein decreased cellular calcium in Ang II-induced VSMCs; furthermore, a Western blot assay indicated that baicalein inhibited the expression of PCNA and significantly lowered levels of phospho-Akt and phospho-ERK, along with an increase in baicalein concentration in Ang II-induced VSMCs. Immunofluorescence staining showed that baicalein pretreatment reduced NF-κB nuclear translocation in Ang II-induced VSMCs and furthered the protein expressions of NLRP3 while ASC and caspase-1 were suppressed in a dose-dependent manner. Baicalein pretreatment upregulated Nrf2/HO-1 signaling in Ang II-induced VSMCs. Thus, 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) staining showed that its reactive oxygen species (ROS) production decreased, along with the baicalein pretreatment. Our overall results indicate that baicalein could have therapeutic potential in preventing aneurysm development. Full article
(This article belongs to the Special Issue Pharmacological Modulation of Oxidative Stress)
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Review

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35 pages, 2797 KiB  
Review
Unveiling the Role of Oxidative Stress in Cochlear Hair Cell Death: Prospective Phytochemical Therapeutics against Sensorineural Hearing Loss
by Nicholas B. Gill, Presley D. Dowker-Key, Mark Hedrick and Ahmed Bettaieb
Int. J. Mol. Sci. 2024, 25(8), 4272; https://doi.org/10.3390/ijms25084272 - 12 Apr 2024
Viewed by 449
Abstract
Hearing loss represents a multifaceted and pervasive challenge that deeply impacts various aspects of an individual’s life, spanning psychological, emotional, social, and economic realms. Understanding the molecular underpinnings that orchestrate hearing loss remains paramount in the quest for effective therapeutic strategies. This review [...] Read more.
Hearing loss represents a multifaceted and pervasive challenge that deeply impacts various aspects of an individual’s life, spanning psychological, emotional, social, and economic realms. Understanding the molecular underpinnings that orchestrate hearing loss remains paramount in the quest for effective therapeutic strategies. This review aims to expound upon the physiological, biochemical, and molecular aspects of hearing loss, with a specific focus on its correlation with diabetes. Within this context, phytochemicals have surfaced as prospective contenders in the pursuit of potential adjuvant therapies. These compounds exhibit noteworthy antioxidant and anti-inflammatory properties, which hold the potential to counteract the detrimental effects induced by oxidative stress and inflammation—prominent contributors to hearing impairment. Furthermore, this review offers an up-to-date exploration of the diverse molecular pathways modulated by these compounds. However, the dynamic landscape of their efficacy warrants recognition as an ongoing investigative topic, inherently contingent upon specific experimental models. Ultimately, to ascertain the genuine potential of phytochemicals as agents in hearing loss treatment, a comprehensive grasp of the molecular mechanisms at play, coupled with rigorous clinical investigations, stands as an imperative quest. Full article
(This article belongs to the Special Issue Pharmacological Modulation of Oxidative Stress)
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17 pages, 1438 KiB  
Review
Nrf2 Pathway in Huntington’s Disease (HD): What Is Its Role?
by Paolo Tucci, Roberta Lattanzi, Cinzia Severini and Luciano Saso
Int. J. Mol. Sci. 2022, 23(23), 15272; https://doi.org/10.3390/ijms232315272 - 03 Dec 2022
Cited by 7 | Viewed by 2358
Abstract
Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease that occurs worldwide. Despite some progress in understanding the onset of HD, drugs that block or delay symptoms are still not available. In recent years, many treatments have been proposed; among them, nuclear transcriptional [...] Read more.
Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease that occurs worldwide. Despite some progress in understanding the onset of HD, drugs that block or delay symptoms are still not available. In recent years, many treatments have been proposed; among them, nuclear transcriptional factor-2 (Nrf2) enhancer compounds have been proposed as potential therapeutic agents to treat HD. Nrf2 triggers an endogenous antioxidant pathway activated in different neurodegenerative disorders. Probably, the stimulation of Nrf2 during either the early phase or before HD symptoms’ onset, could slow or prevent striatum degeneration. In this review, we present the scientific literature supporting the role of Nrf2 in HD and the potential prophylactic and therapeutic role of this compound. Full article
(This article belongs to the Special Issue Pharmacological Modulation of Oxidative Stress)
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