Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
12.4
6.6
Journals
Antioxidants
Special Issues
Antioxidant Therapies, Mitochondrial Function, and Transplantation Strategies: Mechanisms and Emerging...
share announcement

Antioxidant Therapies, Mitochondrial Function, and Transplantation Strategies: Mechanisms and Emerging Therapeutics

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 2811

Special Issue Editors

Dr. Junhwan Kim

E-Mail Website
Guest Editor
Center for Immunology and Inflammation, Feinstein Institutes for Medical Research, Manhasset, NY, USA
Interests: lysophospholipids; LC-MS; diagnosis; lipidomics; ovarian cancer; ROS
Dr. P. Singh

E-Mail
Guest Editor Assistant
Northwell Health, New York, NY, USA
Interests: clinical; chronic disease

Special Issue Information

Dear Colleagues,

Oxidative stress plays a central role in the pathogenesis of numerous acute and chronic diseases. While conventional antioxidant therapies have shown limited clinical utility, recent advances in targeted and mechanistically informed antioxidant strategies are renewing interest in their therapeutic use. Mitochondria, as key regulators of cellular energy and redox homeostasis, are both major sources and targets of oxidative stress, and as our understanding of mitochondrial biology deepens, novel interventions aimed at improving mitochondrial function are gaining attention. Among them, mitochondrial transplantation (MTx)—the transfer of healthy mitochondria into damaged tissues—has emerged as a promising regenerative strategy across a range of human pathologic conditions.

This Special Issue invites original research, comprehensive reviews, and translational perspectives on the following three interconnected themes:

(1) The development and application of antioxidant therapies;

(2) Mechanisms and modulators of mitochondrial function and dysfunction;

(3) Advancements in mitochondrial transplantation technologies.

Submissions addressing each of these topics independently, or exploring their mechanistic interplay, are particularly encouraged.

Dr. Junhwan Kim
Guest Editor

Dr. P. Singh
Guest Editor Assistant

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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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
  • antioxidant therapies
  • mitochondrial function
  • mitochondrial dysfunction

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

19 pages, 8461 KB  
Article
Mitochondria-Associated mRNAs Restore ATP During Oxidative Stress via Cytosolic Translation
by Dong-Bin Back, Gen Hamanaka, Ji-Hyun Park, Shin Ishikane, Masayoshi Tanaka, Takafumi Nakano, Yoshihiko Nakamura and Kazuhide Hayakawa
Antioxidants 2026, 15(5), 580; https://doi.org/10.3390/antiox15050580 - 3 May 2026
Viewed by 526
Abstract
Mitochondrial transplantation has been proposed as a strategy to restore cellular bioenergetics after oxidative injury, but the mechanisms governing ATP recovery remain unclear. Using placental mitochondria, we examined ATP restoration following H2O2-induced oxidative stress. Unmodified mitochondria modestly increased ATP [...] Read more.
Mitochondrial transplantation has been proposed as a strategy to restore cellular bioenergetics after oxidative injury, but the mechanisms governing ATP recovery remain unclear. Using placental mitochondria, we examined ATP restoration following H2O2-induced oxidative stress. Unmodified mitochondria modestly increased ATP under baseline conditions but failed to restore ATP after injury. In contrast, lipid-coated mitochondria (MitoCoat) and lipid-encapsulated mitochondria-associated mRNAs (MitoCoat–mRNA) significantly increased ATP levels in injured cells. Transcriptomic analyses revealed that ATP recovery occurred without the normalization of canonical glycolytic or oxidative phosphorylation (OXPHOS) gene programs. Instead, unmodified mitochondria induced broad transcriptional responses associated with immune activation and cellular stress, whereas MitoCoat elicited a more restricted transcriptional profile. Notably, mitochondria-associated mRNAs alone restored ATP without detectable changes in host transcriptional programs. The removal of mitochondrial surface-associated ribosomes or the inhibition of cytosolic but not mitochondrial translation attenuated ATP recovery. The restoration of key metabolic enzymes through cytosolic translation, including PFKP, pyruvate dehydrogenase, and ATP synthase subunit ATP5A suggests that mitochondria-associated mRNAs promote recovery by re-establishing coupling between glycolysis and mitochondrial OXPHOS. Together, these findings identify encapsulated mitochondria-associated mRNAs as a potential strategy to restore cellular bioenergetics under oxidative stress. Full article
(This article belongs to the Special Issue Antioxidant Therapies, Mitochondrial Function, and Transplantation Strategies: Mechanisms and Emerging Therapeutics)
►▼ Show Figures

Figure 1

33 pages, 7784 KB  
Article
Enriched Environment Suppresses Neuronal Ferroptosis Through SIRT1/AKT/GSK3β-Dependent Glycogen Metabolic Reprogramming After Cerebral Ischemia–Reperfusion
by Bao Zhou, Yixi Hao, Pengkun Yang, Haocheng Qin, Zheng Zhang, Na Ren, Lu Sun, Zhengran Ding, Zhong He, Shuai Zhang, Zijian Hua, Ya Zheng, Ce Li, Shenyi Kuang, Yulian Zhu and Kewei Yu
Antioxidants 2026, 15(5), 570; https://doi.org/10.3390/antiox15050570 - 30 Apr 2026
Viewed by 455
Abstract
Neuronal ferroptosis is a key contributor to secondary brain injury following cerebral ischemia, yet the metabolic mechanisms governing this process remain poorly understood. Enriched environment (EE) is a housing paradigm that provides enhanced sensory, cognitive, and social stimulation through complex physical surroundings and [...] Read more.
Neuronal ferroptosis is a key contributor to secondary brain injury following cerebral ischemia, yet the metabolic mechanisms governing this process remain poorly understood. Enriched environment (EE) is a housing paradigm that provides enhanced sensory, cognitive, and social stimulation through complex physical surroundings and increased opportunities for voluntary activity. Our preliminary data indicate that EE confers cerebroprotection against ischemia-induced ferroptosis; however, whether this effect is associated with glycogen metabolic regulation and the underlying molecular pathways has not been elucidated. This study aimed to determine whether EE may influence ferroptosis-associated pathways, potentially via Sirtuin 1 (SIRT1)/protein kinase B (AKT)/glycogen synthase kinase-3β (GSK3β)-related mechanisms of glycogen metabolism. Using a mouse model of middle cerebral artery occlusion (MCAO) and an oxygen–glucose deprivation/reoxygenation (OGD/R) cellular model, we performed behavioral assessments, molecular and biochemical analyses, and pharmacological interventions to elucidate mechanistic pathways. EE was associated with improved neurological outcomes and reduced infarct volume after ischemia. Mechanistically, EE appeared to activate the SIRT1/AKT pathway and increase the inhibitory phosphorylation of GSK3β and relieving its suppressive effect on glycogen synthase, which may underlie the observed increase in glycogen levels within ischemic brain tissue. Pharmacological inhibition of SIRT1 largely diminished these metabolic and neuroprotective benefits. Consistently, at the cellular level, SIRT1 overexpression contributed to the restoration of glycogen metabolism and robustly attenuated ferroptosis under ischemic conditions. Collectively, these findings suggest that EE may attenuate ferroptosis-related pathways possibly involving SIRT1/AKT/GSK3β-dependent glycogen metabolic remodeling, providing a novel metabolic perspective on EE-induced cerebroprotection and highlighting SIRT1-centered regulation of glycogen metabolism as a potential therapeutic target for ischemic stroke. Full article
(This article belongs to the Special Issue Antioxidant Therapies, Mitochondrial Function, and Transplantation Strategies: Mechanisms and Emerging Therapeutics)
►▼ Show Figures

Graphical abstract

29 pages, 8236 KB  
Article
Enriched Environment Ameliorates Cerebral Ischemia–Reperfusion Injury via Dopamine–H2S Axis-Mediated Dual Mitophagy Activation
by Bao Zhou, Haocheng Qin, Pengkun Yang, Na Ren, Lu Sun, Zhengran Ding, Zhong He, Shuai Zhang, Zijian Hua, Ya Zheng, Ce Li, Shenyi Kuang, Yulian Zhu and Kewei Yu
Antioxidants 2026, 15(1), 52; https://doi.org/10.3390/antiox15010052 - 30 Dec 2025
Cited by 1 | Viewed by 1184
Abstract
Cerebral ischemia–reperfusion injury triggers mitochondrial dysfunction and oxidative stress, exacerbating neuronal apoptosis. Emerging evidence highlights hydrogen sulfide (H2S) as a gasotransmitter modulating redox balance, autophagy, and apoptosis. This study investigates the neuroprotective mechanisms of Enriched Environment (EE) against ischemic injury, focusing [...] Read more.
Cerebral ischemia–reperfusion injury triggers mitochondrial dysfunction and oxidative stress, exacerbating neuronal apoptosis. Emerging evidence highlights hydrogen sulfide (H2S) as a gasotransmitter modulating redox balance, autophagy, and apoptosis. This study investigates the neuroprotective mechanisms of Enriched Environment (EE) against ischemic injury, focusing on mitochondrial dynamics and H2S-mediated pathways. Using MCAO mice and OGD/R-treated SH-SY5Y neurons, interventions targeting H2S synthesis, hypoxia-inducible factor 1-alpha (HIF-1α), and mitophagy were implemented. Behavioral, histological, and molecular analyses demonstrated EE significantly improved neurological outcomes, suppressed apoptosis, and attenuated oxidative damage (reduced MDA, elevated MnSOD/glutathione). Mechanistically, EE enhanced mitophagy via dual pathways: canonical PINK1/parkin-mediated mitochondrial clearance, corroborated by transmission electron microscope and LC3B/parkin colocalization, and non-canonical HIF-1α/BNIP3L axis activation. Transcriptomic and Co-immunoprecipitation (Co-IP) data revealed EE upregulated endogenous H2S biosynthesis post-injury by promoting dopamine-induced calcium influx, which activated calmodulin-dependent signaling to stimulate cystathionine β-synthase/γ-lyase expression. Pharmacological blockade of H2S synthesis or HIF-1α abolished mitochondrial protection, confirming H2S as a central mediator. Notably, H2S exerted antiapoptotic effects by restoring mitochondrial integrity through synergistic mitophagy activation and oxidative stress mitigation. These findings propose a novel neuroprotective cascade: EE-induced dopaminergic signaling potentiates H2S production, which coordinates PINK1/parkin and HIF-1α/BNIP3L pathways to eliminate dysfunctional mitochondria, thereby preserving neuronal homeostasis. This study elucidates therapeutic potential of EE via H2S-driven mitochondrial quality control, offering insights for ischemic brain injury intervention. Full article
(This article belongs to the Special Issue Antioxidant Therapies, Mitochondrial Function, and Transplantation Strategies: Mechanisms and Emerging Therapeutics)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop