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Autophagy and Cellular Oxidative Stress: Molecular Mechanisms and Diagnostic Biomarkers
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Autophagy and Cellular Oxidative Stress: Molecular Mechanisms and Diagnostic Biomarkers

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

Deadline for manuscript submissions: 20 February 2025 | Viewed by 3143

Special Issue Editors

Dr. Ramona D’Amico

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy
Interests: inflammation; oxidative stress; reactive oxygen species; cytokines storm; molecular pathways; in vivo models; natural compounds
Dr. Daniela Impellizzeri

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Via F. Stagno D’Alcontres 31, 98166 Messina, Italy
Interests: inflammation; oxidative stress; biochemistry; pharmacology; molecular biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The objective of this Special Issue is to improve our knowledge regarding the cellular and molecular mechanisms involved in autophagy and oxidative stress. Oxidative stress and redox signaling are largely involved in the etiology of human diseases, where both survival and cell death signaling cascades have been reported to be modulated by reactive oxygen species (ROS) and reactive nitrogen species (RNS). ROS and RNS activate autophagy, which facilitates cellular adaptation and diminishes oxidative damage by degrading and recycling intracellular damaged macromolecules and dysfunctional organelles; therefore, autophagy is a major cellular defense against oxidative stress, or related conditions that cause accumulation of damaged proteins or organelles.

This Special Issue, presided by Dr. Daniela Impellizzeri and Ramona D’Amico as Guest Editor, and Dr. Rosalba Siracusa as Topical Advisory Panel Member. We welcome research aimed at improving our understanding of molecular mechanisms and biomarkers through which oxidative stress and autophagy regulate human disease. Indeed, the identification of specific biomarkers of oxidative stress and autophagy is of great importance for disease prevention, monitoring disease progression and evaluating the effectiveness of treatments.

We welcome various types of manuscripts, including original research and review articles, clinical trials and instructive case reports.

Dr. Ramona D’Amico
Dr. Daniela Impellizzeri
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

  • autophagy
  • oxidative stress
  • biomarkers
  • acute and chronic diseases
  • molecular pathways
  • ROS
  • mitophagy

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Published Papers (3 papers)

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Research

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13 pages, 4286 KiB  
Article
A Selective Melatonin 2 Receptor Agonist, IIK7, Relieves Blue Light-Induced Corneal Damage by Modulating the Process of Autophagy and Apoptosis
by Hyeon-Jeong Yoon, Enying Jiang, Jingting Liu, Hui Jin, Hee Su Yoon, Ji Suk Choi, Ja Young Moon and Kyung Chul Yoon
Int. J. Mol. Sci. 2024, 25(20), 11243; https://doi.org/10.3390/ijms252011243 - 19 Oct 2024
Viewed by 802
Abstract
This study aims to investigate the effect of the selective MT2 receptor agonist, IIK7, on corneal autophagy and apoptosis, aiming to reduce corneal epithelial damage and inflammation from blue light exposure in mice. Eight-week-old C57BL/6 mice were divided into BL-exposed (BL) and BL-exposed [...] Read more.
This study aims to investigate the effect of the selective MT2 receptor agonist, IIK7, on corneal autophagy and apoptosis, aiming to reduce corneal epithelial damage and inflammation from blue light exposure in mice. Eight-week-old C57BL/6 mice were divided into BL-exposed (BL) and BL-exposed with IIK7 treatment (BL + IIK7 group). Mice underwent blue light exposure (410 nm, 100 J) twice daily with assessments at baseline and on days 3, 7, and 14. Corneal samples were analyzed for MT2 receptor expression, autophagy markers (LC3-II and p62), and apoptosis indicators (BAX expression and TUNEL assay). Then, mice were assigned to normal control, BL, and BL + IIK7. Ocular surface parameters, including corneal fluorescein staining scores, tear volume, and tear film break-up time, were evaluated on days 7 and 14. On day 14, reactive oxygen species (ROS) levels and CD4+ IFN-γ+ T cells percentages were measured. The BL group exhibited higher LC3-II and p62 expression, while the BL + IIK7 group showed reduced expression (p < 0.05). The TUNEL assay showed reduced apoptosis in the BL + IIK7 group compared to the BL group. ROS levels were lower in the BL + IIK7 group. The BL + IIK7 group showed improved ocular surface parameters, including decreased corneal fluorescein staining and increased tear volume. The percentages of CD4+ IFN-γ+ T cells indicated reduced inflammatory responses in the BL + IIK7 group. The MT2 receptor agonist IIK7 regulates corneal autophagy and apoptosis, reducing corneal epithelial damage and inflammation from blue light exposure. Full article
(This article belongs to the Special Issue Autophagy and Cellular Oxidative Stress: Molecular Mechanisms and Diagnostic Biomarkers)
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15 pages, 6890 KiB  
Article
c-Jun N-terminal Kinase Supports Autophagy in Testicular Ischemia but Triggers Apoptosis in Ischemia-Reperfusion Injury
by Sarah R. Alotaibi, Waleed M. Renno and May Al-Maghrebi
Int. J. Mol. Sci. 2024, 25(19), 10446; https://doi.org/10.3390/ijms251910446 - 27 Sep 2024
Viewed by 633
Abstract
Oxidative stress triggered by testicular torsion and detorsion in young males could negatively impact future fertility. Using a rat animal model for testicular IRI (tIRI), we aim to study the induction of autophagy (ATG) during testicular ischemia and tIRI and the role of [...] Read more.
Oxidative stress triggered by testicular torsion and detorsion in young males could negatively impact future fertility. Using a rat animal model for testicular IRI (tIRI), we aim to study the induction of autophagy (ATG) during testicular ischemia and tIRI and the role of oxidative-stress-induced c-Jun N-terminal Kinase (JNK) as a cytoprotective mechanism. Sixty male Sprague-Dawley rats were divided into five groups: sham, ischemia only, ischemia+SP600125 (a JNK inhibitor), tIRI only, and tIRI+SP600125. The tIRI rats underwent an ischemic injury for 1 h followed by 4 h of reperfusion, while ischemic rats were subjected to 1 h of ischemia only without reperfusion. Testicular-ischemia-induced Beclin 1 and LC3B expression was associated with decreased p62/SQSTM1 expression, increased ATP and alkaline phosphatase (AP) activity, and slightly impaired spermatogenesis. SP600125 treatment improved p62 expression and reduced the levels of Beclin 1 and LC3B but did not affect ATP or AP levels. The tIRI-induced apoptosis lowered the expression of the three ATG proteins and AP activity, activated caspase 3, and caused spermatogenic arrest. SP600125-inhibited JNK during tIRI restored sham levels to all investigated parameters. This study emphasizes the regulatory role of JNK in balancing autophagy and apoptosis during testicular oxidative injuries. Full article
(This article belongs to the Special Issue Autophagy and Cellular Oxidative Stress: Molecular Mechanisms and Diagnostic Biomarkers)
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Review

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33 pages, 1919 KiB  
Review
The Interplay between Autophagy and Mitochondria in Cancer
by Aleksandra Zdanowicz and Emilia Grosicka-Maciąg
Int. J. Mol. Sci. 2024, 25(17), 9143; https://doi.org/10.3390/ijms25179143 - 23 Aug 2024
Viewed by 1349
Abstract
Besides producing cellular energy, mitochondria are crucial in controlling oxidative stress and modulating cellular metabolism, particularly under stressful conditions. A key aspect of this regulatory role involves the recycling process of autophagy, which helps to sustain energy homeostasis. Autophagy, a lysosome-dependent degradation pathway, [...] Read more.
Besides producing cellular energy, mitochondria are crucial in controlling oxidative stress and modulating cellular metabolism, particularly under stressful conditions. A key aspect of this regulatory role involves the recycling process of autophagy, which helps to sustain energy homeostasis. Autophagy, a lysosome-dependent degradation pathway, plays a fundamental role in maintaining cellular homeostasis by degrading damaged organelles and misfolded proteins. In the context of tumor formation, autophagy significantly influences cancer metabolism and chemotherapy resistance, contributing to both tumor suppression and surveillance. This review focuses on the relationship between mitochondria and autophagy, specifically in the context of cancer progression. Investigating the interaction between autophagy and mitochondria reveals new possibilities for cancer treatments and may result in the development of more effective therapies targeting mitochondria, which could have significant implications for cancer treatment. Additionally, this review highlights the increasing understanding of autophagy’s role in tumor development, with a focus on modulating mitochondrial function and autophagy in both pre-clinical and clinical cancer research. It also explores the potential for developing more-targeted and personalized therapies by investigating autophagy-related biomarkers. Full article
(This article belongs to the Special Issue Autophagy and Cellular Oxidative Stress: Molecular Mechanisms and Diagnostic Biomarkers)
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