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Programmed Cell Death and Oxidative Stress: 4th Edition
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Programmed Cell Death and Oxidative Stress: 4th Edition

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 August 2026) | Viewed by 1619

Editor

Dr. Takuya Noguchi

E-Mail Website
Guest Editor
Department of Biopharmaceutical Science, Tohoku University, Sendai 980-8578, Japan
Interests: apoptosis; signaling pathways; phosphorylation; signal transduction; cell signaling; reactive oxygen species; molecular cell biology; cell biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue “Programmed Cell Death and Oxidative Stress: 3rd Edition” (https://www.mdpi.com/journal/ijms/special_issues/J3EREAR20U).

Cells that constitute aerobic organisms are continuously exposed to reactive oxygen species (ROS), whose accumulation often initiates oxidative stress. Importantly, oxidative stress plays a critical role in the determination of cell fate by inducing cellular responses, such as proliferation, differentiation and programmed cell death. Accumulating evidence indicates that oxidative stress initiates various forms of programmed cell death including apoptosis, necroptosis, pyroptosis, parthanatos and ferroptosis. Moreover, all types of oxidative-stress-induced cell deaths are closely associated with a wide variety of diseases. For this Special Issue, studies of a wide range of signaling mechanisms and pathological processes related to oxidative-stress-induced cell death are welcome.

Dr. Takuya Noguchi
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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
  • programmed cell death
  • cellular stresses
  • senescence
  • cytotoxicity
  • cancer
  • neurodegenerative disease
  • inflammatory disease
  • organelle stress

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Published Papers (3 papers)

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Research

15 pages, 1902 KB  
Article
Protective Effects of Ranolazine in a Rat Model of Ovarian Ischemia/Reperfusion Injury
by Mesut Admis, Esra Tuba Sezgin, Zeynep Suleyman, Ozlem Admis, Mustafa Ozkaraca, Ali Gungor, Aydin Aliyev and Halis Suleyman
Int. J. Mol. Sci. 2026, 27(15), 7023; https://doi.org/10.3390/ijms27157023 - 5 Aug 2026
Viewed by 401
Abstract
Ovarian ischemia/reperfusion (I/R) injury is a major cause of tissue damage following the surgical detorsion of ovarian torsion and is characterized by excessive oxidative stress, inflammation, and progressive cellular injury. Although ranolazine has been reported to exert antioxidant and anti-inflammatory effects in various [...] Read more.
Ovarian ischemia/reperfusion (I/R) injury is a major cause of tissue damage following the surgical detorsion of ovarian torsion and is characterized by excessive oxidative stress, inflammation, and progressive cellular injury. Although ranolazine has been reported to exert antioxidant and anti-inflammatory effects in various experimental models, its potential protective effects against ovarian I/R injury have not yet been investigated. This study aimed to evaluate whether pretreatment with ranolazine protects ovarian tissue against experimental I/R injury in rats. Twenty-four female Wistar albino rats were randomly assigned to four groups: a healthy group (HG), sham-operated group (SOG), ovarian ischemia/reperfusion (OIR) group, and ranolazine-treated ovarian ischemia/reperfusion (ROIR) group. Ovarian ischemia was induced by 1 h of torsion followed by 6 h of reperfusion. Ranolazine (50 mg/kg) was administered 1 h before the induction of ischemia as a preventive pretreatment. Oxidative stress markers (MDA, tGSH, SOD, and CAT), pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), histopathological alterations, and the expression of COX-1, COX-2, IL-1β, and IL-6 were evaluated by double immunofluorescence staining. Ovarian I/R significantly increased MDA and pro-inflammatory cytokine levels while markedly decreasing tGSH levels and SOD and CAT activities (p < 0.001). These biochemical alterations were accompanied by severe follicular degeneration, mononuclear cell infiltration, interstitial edema, decreased COX-1 immunoreactivity, and increased expression of COX-2, IL-1β, and IL-6. Ranolazine treatment significantly attenuated oxidative stress and inflammatory responses, preserved the antioxidant defense system, ameliorated histopathological damage, restored COX-1 immunoreactivity, and inhibited the expression of COX-2, IL-1β, and IL-6. This is the first experimental study evaluating ranolazine in ovarian I/R injury. These findings suggest that preventive pretreatment with ranolazine attenuates experimental ovarian I/R injury through antioxidant and anti-inflammatory mechanisms. Future studies are needed to determine whether similar protective effects can be achieved when ranolazine is administered after ovarian torsion or following surgical detorsion. Full article
(This article belongs to the Special Issue Programmed Cell Death and Oxidative Stress: 4th Edition)
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21 pages, 10917 KB  
Article
Bakuchiol Enhances 5-Fluorouracil Efficacy in Colorectal Cancer Cells via a ROS-Dependent Mechanism Involving Mitochondrial Dysfunction and Apoptosis
by Dominika Radomska, Olga Szewczyk-Roszczenko, Magda Chalecka, Arkadiusz Surazynski, Anna Szymanowska, Krzysztof Bielawski and Robert Czarnomysy
Int. J. Mol. Sci. 2026, 27(13), 5894; https://doi.org/10.3390/ijms27135894 - 30 Jun 2026
Viewed by 431
Abstract
Resistance to 5-fluorouracil (5-FU) remains a major limitation in colorectal cancer therapy, prompting the development of combination strategies aimed at improving its efficacy. Bakuchiol (BAK), a natural compound with reported antioxidant and pro-oxidant properties, may modulate redox balance and enhance chemotherapy response. This [...] Read more.
Resistance to 5-fluorouracil (5-FU) remains a major limitation in colorectal cancer therapy, prompting the development of combination strategies aimed at improving its efficacy. Bakuchiol (BAK), a natural compound with reported antioxidant and pro-oxidant properties, may modulate redox balance and enhance chemotherapy response. This study compared the effects of 5-FU and BAK, applied as monotherapies and in combination, in DLD-1 and HT-29 colorectal cancer cells. Cytotoxicity assays showed that co-treatment significantly reduced the IC50 of 5-FU, particularly in DLD-1 cells, and revealed an enhanced anticancer effect of the combination treatment compared with either monotherapy. Flow cytometric analyses demonstrated enhanced apoptosis via extrinsic and intrinsic pathways, including increased caspase 8 activity, loss of mitochondrial membrane potential (ΔΨm), activation of caspase 9, and subsequent activation of caspases 3/7. These effects were associated with a pronounced redox imbalance, reflected by increased intracellular reactive oxygen species (ROS) levels, suggesting a central role of oxidative stress in mediating cytotoxicity. Antioxidant pre-treatment attenuated ROS accumulation and reduced apoptosis, confirming a causal relationship. Additionally, autophagy was induced selectively in DLD-1 cells, indicating cell-line-specific differences in redox adaptation. Taken together, BAK enhances 5-FU efficacy through ROS-dependent activation of mitochondrial and caspase-dependent pathways, with stronger effects observed in DLD-1 cells. Full article
(This article belongs to the Special Issue Programmed Cell Death and Oxidative Stress: 4th Edition)
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21 pages, 17327 KB  
Article
Protective Effects of Selective β-Adrenoceptor Blockade on Renal Pathophysiology in a Catecholamine Storm of Rat
by Bo-Hau Chen, Tzu-Hao Liu, Guan-Hong Lin, Hsin-Hung Chen, Yi-Ting Chu, Chih-Chieh Yang and Wen-Hsien Lu
Int. J. Mol. Sci. 2026, 27(12), 5480; https://doi.org/10.3390/ijms27125480 - 17 Jun 2026
Viewed by 429
Abstract
Excessive administration of epinephrine and norepinephrine in critically ill patients may trigger a catecholamine storm and contribute to acute kidney injury (AKI) through activation of β-adrenoceptor signaling. Although clinical observations link high-dose catecholamine exposure to increased AKI risk, experimental models and mechanistic studies [...] Read more.
Excessive administration of epinephrine and norepinephrine in critically ill patients may trigger a catecholamine storm and contribute to acute kidney injury (AKI) through activation of β-adrenoceptor signaling. Although clinical observations link high-dose catecholamine exposure to increased AKI risk, experimental models and mechanistic studies remain limited. We established a rodent model of combined epinephrine and norepinephrine infusion to investigate the renoprotective effects of subtype-selective β-adrenoceptor blockers. Animals received the β1-selective blockers metoprolol or atenolol, or the β2-selective blocker ICI 118,551. β1-adrenoceptor blockade, particularly with metoprolol, significantly attenuated renal histopathological injury and improved biochemical markers of kidney dysfunction. These protective effects were associated with suppression of ferroptosis-related pathways in the renal cortex. Atenolol partially improved biochemical parameters but did not significantly reduce tubulointerstitial damage, whereas β2-adrenoceptor blockade conferred limited functional benefit despite modest morphological improvement. Collectively, our findings indicate that β1-adrenoceptor activation plays a critical role in catecholamine-induced AKI by promoting ferroptosis. Targeting β1-adrenoceptors, especially with metoprolol, may represent a potential therapeutic strategy for preventing renal injury during catecholamine storms. Full article
(This article belongs to the Special Issue Programmed Cell Death and Oxidative Stress: 4th Edition)
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