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Oxidative Stress and Cell Damage
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Oxidative Stress and Cell Damage

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 September 2025 | Viewed by 4234

Special Issue Editors

Prof. Dr. Haruhiko Inufusa

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Guest Editor
Division of Antioxidant Research, Gifu University, Gifu, Japan
Interests: oxidative stress; antioxidants; cancer
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Koji Abe

E-Mail Website
Guest Editor
Tokyo Reborn Clinic Ginza, 1-15-4 Ginza, Chu-ku, Tokyo 1040061, Japan
Interests: oxidative stress; neuro degradative disease; dementia; brain stroke
Prof. Dr. Shigeru Hirano

E-Mail Website
Guest Editor
Department of Otolaryngology-Head and Neck Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan
Interests: oxidative stress; hearing loss; vocal code damage
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, research into oxidative stress and disease has progressed, and the role and importance of oxidative stress in a wide variety of diseases has become clear. However, the development of convenient oxidative stress markers and safe antioxidant treatment methods is not sufficient. In this special issue, we are looking for manuscripts on a wide range of topics, including: 1. The effects of oxidative stress on cells, organs and the human body; 2. Tests and phenomena that can be used as indicators of oxidative stress; 3. Disease prevention; 4. Protection of cells from oxidative stress and disease prevention; and 5. New findings on oxidative stress.

Prof. Dr. Haruhiko Inufusa
Prof. Dr. Koji Abe
Prof. Dr. Shigeru Hirano
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

  • oxidative stress
  • damages on cells, organs, body
  • prevention damages
  • parameter of oxidative stress
  • antioxidants

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Published Papers (2 papers)

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Review

14 pages, 392 KiB  
Review
Noise-Induced Hearing Loss: Overview and Future Prospects for Research on Oxidative Stress
by Tsubasa Kitama, Takanori Nishiyama, Makoto Hosoya, Marie N. Shimanuki, Masafumi Ueno, Fukka You, Hiroyuki Ozawa and Naoki Oishi
Int. J. Mol. Sci. 2025, 26(10), 4927; https://doi.org/10.3390/ijms26104927 - 21 May 2025
Viewed by 295
Abstract
Noise-induced hearing loss (NIHL) is a common type of sensorineural hearing loss caused by exposure to high-intensity noise that leads to irreversible cochlear damage. Despite extensive research on cochlear pathophysiology, the precise mechanisms remain unclear, and no established treatment exists. This is due [...] Read more.
Noise-induced hearing loss (NIHL) is a common type of sensorineural hearing loss caused by exposure to high-intensity noise that leads to irreversible cochlear damage. Despite extensive research on cochlear pathophysiology, the precise mechanisms remain unclear, and no established treatment exists. This is due to the challenges in imaging and the inability to perform biopsies in human patients. Consequently, animal models, particularly mice, have been widely used to study NIHL. Clinically, NIHL presents as either a temporary threshold shift, in which hearing recovers, or a permanent threshold shift, which results in an irreversible loss. Histopathological studies have identified the key features of NIHL, including outer hair cell loss, auditory nerve degeneration, and synaptic impairment. Recent findings suggest that oxidative stress and inflammation are major contributors to NIHL, highlighting the potential for therapeutic interventions, such as antioxidants and anti-inflammatory agents. Given the increasing prevalence of NIHL owing to occupational noise exposure and personal audio device use, addressing this issue is a pressing public health challenge. This review summarizes the clinical features, underlying mechanisms, and emerging treatment strategies for NIHL while identifying current knowledge gaps and future research directions. Full article
(This article belongs to the Special Issue Oxidative Stress and Cell Damage)
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35 pages, 2760 KiB  
Review
The Unified Theory of Neurodegeneration Pathogenesis Based on Axon Deamidation
by Davis Joseph
Int. J. Mol. Sci. 2025, 26(9), 4143; https://doi.org/10.3390/ijms26094143 - 27 Apr 2025
Viewed by 3235
Abstract
Until now, neurodegenerative diseases like Alzheimer’s and Parkinson’s have been studied separately in biochemistry and therapeutic drug development, and no causal link has ever been established between them. This study has developed a Unified Theory, which establishes that the regulation of axon and [...] Read more.
Until now, neurodegenerative diseases like Alzheimer’s and Parkinson’s have been studied separately in biochemistry and therapeutic drug development, and no causal link has ever been established between them. This study has developed a Unified Theory, which establishes that the regulation of axon and dendrite-specific 4E-BP2 deamidation rates controls the occurrence and progression of neurodegenerative diseases. This is based on identifying axon-specific 4E-BP2 deamidation as a universal denominator for the biochemical processes of deamidation, translational control, oxidative stress, and neurodegeneration. This was achieved by conducting a thorough and critical review of 224 scientific publications regarding (a) deamidation, (b) translational control in protein synthesis initiation, (c) neurodegeneration and (d) oxidative stress, and by applying my discovery of the fundamental neurobiological mechanism behind neuron-specific 4E-BP2 deamidation to practical applications in medicine. Based on this newly developed Unified Theory and my critical review of the scientific literature, I also designed three biochemical flowsheets of (1) in-vivo deamidation, (2) protein synthesis initiation and translational control, and (3) 4E-BP2 deamidation as a control system of the four biochemical processes. The Unified Theory of Neurodegeneration Pathogenesis based on axon deamidation, developed in this work, paves the way to controlling the occurrence and progression of neurodegenerative diseases such as Alzheimer’s and Parkinson’s through a unique, neuron-specific regulatory system that is 4E-BP2 deamidation, caused by the proteasome-poor environment in neuronal projections, consisting mainly of axons. Full article
(This article belongs to the Special Issue Oxidative Stress and Cell Damage)
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