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Cells
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The Role of Mitochondria in Health, Disease, and Ageing
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The Role of Mitochondria in Health, Disease, and Ageing

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Mitochondria".

Deadline for manuscript submissions: 10 July 2026 | Viewed by 1142

Special Issue Editors

Dr. Arunkumar Venkatesan

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Guest Editor
Department of Ophthalmology and Visual Sciences, SUNY Upstate Medical University, Syracuse, NY, USA
Interests: mitochondria; protein folding; aggregation; protein quality control and degradation
Prof. Dr. Ritva Tikkanen

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Guest Editor
Institute of Biochemistry, Medical Faculty, Justus-Liebig University of Giessen, Friedrichstrasse 24, D-35392 Giessen, Germany
Interests: lysosomal storage disorders; vesicular trafficking; endosomal sorting; lysosome biogenesis; mitochondrial diseases; autoimmune disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are pivotal regulators of energy production, cellular metabolism, and cell growth, and they also contribute to proteostasis and cellular signaling. Their roles further encompass the regulation of calcium homeostasis, mitochondrial biomolecule synthesis, and the orchestration of different forms of cell death and differentiation. Because of these versatile roles, mitochondrial health is foundational to cellular integrity, and any defects in mitochondrial function underlie a large spectrum of human diseases, ranging from rare, inherited mitochondrial syndromes to common, acquired disorders of aging and metabolism. Advances in understanding mitochondrial function and dysfunction offer unparalleled opportunities to develop mitochondria-targeted therapeutics and interventions to improve patient outcomes.

This Special Issue aims to highlight cutting-edge achievements in mitochondrial research concerning health and disease across various inherited and acquired mitochondrial disorders, as well as in the ageing process. Key themes may include, but are not limited to, the biochemistry and molecular biology of mitochondria, crosstalk between mitochondria and other cellular organelles, the role of mitochondria in aging, molecular mechanisms of mitochondrial dynamics, advances in mtDNA research, oxidative stress and inflammation, mitochondrial metabolic alterations, and new avenues in mitochondrial pathway-targeted therapeutics. We welcome original research, critical reviews, and perspectives that foster new ideas and discoveries in mitochondrial biology and their role in health, disease, and ageing. By bringing together work on both inherited mitochondrial diseases and acquired dysfunctions, this Special Issue aims to define the future directions for mitochondrial research and translational medicine.

Dr. Arunkumar Venkatesan
Prof. Dr. Ritva Tikkanen
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 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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • mitochondrial dysfunction
  • metabolism
  • mitochondrial genetics
  • aging and senescence
  • bioenergetics
  • mitophagy
  • neurodegeneration
  • cardiomyopathy
  • metabolic syndrome
  • ocular diseases

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Published Papers (2 papers)

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Research

20 pages, 5185 KB  
Article
The Upregulation of NDUFB3 Is Implicated in Mitochondrial Dysfunction and Neuronal Apoptosis in Ischemic Stroke
by Shuyue Cheng, Zeyue Mu, Feng Zhang, Jianyou Song, Jiapeng Shao, Yunqi Yan, Anastasios A. Daskalakis, Yunjie Wang, Bin Zhang, Yashuang Jiang, Le Wang and Fang Liu
Cells 2026, 15(12), 1071; https://doi.org/10.3390/cells15121071 (registering DOI) - 12 Jun 2026
Abstract
Background: Mitochondrial dysfunction is a central event in the pathogenesis of ischemic stroke. The roles of specific mitochondrial complex subunits, such as NDUFA4 and NDUFB3, in cerebral ischemia–reperfusion injury remain poorly defined. This study aims to investigate the dynamic expressions and functional impact [...] Read more.
Background: Mitochondrial dysfunction is a central event in the pathogenesis of ischemic stroke. The roles of specific mitochondrial complex subunits, such as NDUFA4 and NDUFB3, in cerebral ischemia–reperfusion injury remain poorly defined. This study aims to investigate the dynamic expressions and functional impact of NDUFA4 and NDUFB3 in ischemic stroke. Methods: A transient middle cerebral artery occlusion (MCAO) model was established in male C57BL/6J mice. Label-free quantitative proteomics and Western blotting were employed to analyze protein expression in the ischemic penumbra. Highly differentiated PC12 cells were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) or glutamate excitotoxicity to mimic ischemic injury in vitro. The functional consequences of NDUFB3 knockdown and overexpression were assessed by measuring ATP levels, reactive oxygen species (ROS), mitochondrial membrane potential (ΔΨm), and apoptosis. The involvement of the JNK-mediated mitochondrial apoptotic pathway was also examined. Results: Proteomic analysis revealed a significant upregulation of NDUFA4 and NDUFB3 in the ischemic penumbra of MCAO mice, as verified by western blot. In highly differentiated PC12 cells, both OGD/R and glutamate exposure induced a time-dependent increase in these proteins in mitochondrial fractions. Functional studies demonstrated that NDUFB3 knockdown significantly rescued OGD/R-induced mitochondrial dysfunction, as indicated by restored ATP production, reduced ROS generation, and stabilized ΔΨm. Furthermore, NDUFB3 silencing attenuated apoptosis by inhibiting JNK phosphorylation and decreasing BAX levels. Conversely, overexpression of NDUFB3 alone was sufficient to induce mitochondrial abnormalities, including loss of ΔΨm and elevated oxidative stress in highly differentiated PC12 cells. Conclusions: Ischemic injury triggers the upregulation of mitochondrial complex subunits NDUFA4 and NDUFB3. While this may initially act as a compensatory response, our findings identify NDUFB3 as a critical mediator of ischemic stroke pathology, whose overexpression drives mitochondrial dysfunction and apoptosis. In contrast, the suppression of NDUFB3 provides protection against ischemic injury. Therefore, NDUFB3 may be a potential candidate therapeutic target for reducing mitochondrial damage in ischemic stroke, but this role requires further validation in additional experimental and translational models. Full article
(This article belongs to the Special Issue The Role of Mitochondria in Health, Disease, and Ageing)
22 pages, 10897 KB  
Article
Inhibitory Effect of ATP on Cytochrome c Oxidase Depends on Electron Entry Pathways by TCA Cycle Metabolites
by Madeline Günther, Valeria Pakic, Petra Weber, Anke Veit, Carsten Culmsee, Ardawan J. Rastan, Annegret P. Busch and Sebastian Vogt
Cells 2026, 15(9), 811; https://doi.org/10.3390/cells15090811 - 29 Apr 2026
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Abstract
The ATP-dependent inhibition of cytochrome c oxidase (CytOx, complex IV of the electron transport chain) is the second mechanism of respiratory control adjusting mitochondrial respiration in order to prevent excessive electron flow and reactive oxygen species (ROS) production. Here, we investigate how tricarboxylic [...] Read more.
The ATP-dependent inhibition of cytochrome c oxidase (CytOx, complex IV of the electron transport chain) is the second mechanism of respiratory control adjusting mitochondrial respiration in order to prevent excessive electron flow and reactive oxygen species (ROS) production. Here, we investigate how tricarboxylic acid (TCA) cycle metabolites and the subsequent complex I or complex II activities influence this regulatory mechanism. Therefore, CytOx activity was assessed by the oxygen consumption rate after cytochrome c (Cyt c) titration to stimulate complex IV activity in isolated rat heart mitochondria (RHM) and permeabilized AC16 cells. Mitochondrial membrane potential (Δψm) and ROS formation were analysed by flow cytometry. Our results show that TCA cycle intermediates differed in their impact on CytOx activity and subsequent ROS formation. NADH-linked substrates such as α-ketoglutarate, glutamate and malate increased respiratory capacity, but preserved ATP-dependent control of CytOx, indicating that elevated electron supply alone does not necessarily abolish ATP sensitivity. In contrast, succinate, which feeds electrons directly into complex II, strongly increased respiration causing the loss of ATP-dependent respiratory control in both model systems. Despite this strong respiratory effect, succinate induced only modest changes in mitochondrial membrane potential in isolated mitochondria, whereas permeabilized cardiomyocytes exhibited reduced polarization accompanied by increased superoxide formation. Together, these findings demonstrate that the effectiveness of ATP-dependent CytOx inhibition is influenced by TCA cycle activity and depends on the site of electron entry into the respiratory chain. Thus, substrate-dependent modulation of respiratory control links metabolite availability to mitochondrial redox regulation in cardiac cells. Full article
(This article belongs to the Special Issue The Role of Mitochondria in Health, Disease, and Ageing)
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