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Mitochondrial Bioenergetics and Signaling in Diseases
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Mitochondrial Bioenergetics and Signaling in Diseases

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

Deadline for manuscript submissions: 28 February 2027 | Viewed by 1698

Editors

Prof. Dr. Carlos Palmeira

E-Mail Website
Guest Editor
Department of Life Sciences and Center for Neurosciences and Cell Biology, University of Coimbra, 3004-531 Coimbra, Portugal
Interests: liver; muscle; adipose tissue; ischemia/reperfusion; mitochondria; steatosis; mitochondrial signaling and bioenergetics; mitochondrial dynamics; mitohormesis
Special Issues, Collections and Topics in MDPI journals
Dr. Anabela P. Rolo

E-Mail Website
Guest Editor
Center for Innovative Biomedicine and Biotechnology (CiBB), University of Coimbra, 3004-504 Coimbra, Portugal
Interests: PCR; electrophoresis; gene expression; molecular biology; cell biology; biochemistry; signal transduction; Western blot; oxidative stress; signaling pathways; liver diseases; mitochondria bioenergetics; mitochondria isolation; liver mitochondria
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are central hubs of cellular energy production and signaling, integrating metabolic demands with stress responses, redox balance and cell fate decisions. Beyond their classical role in ATP synthesis, mitochondria actively participate in signaling pathways that regulate inflammation, apoptosis, immunity and tissue homeostasis. Dysregulation of mitochondrial bioenergetics and signaling has emerged as a unifying mechanism underlying a wide spectrum of human diseases.

This Special Issue focuses on recent advances in understanding how mitochondrial energy metabolism, dynamics and signaling networks contribute to disease initiation and progression. Topics include alterations in oxidative phosphorylation, mitochondrial DNA integrity, metabolite signaling, reactive oxygen species, calcium handling and mitochondrial quality control, as well as crosstalk between mitochondria and other cellular compartments. Particular emphasis is placed on mitochondrial dysfunction in neurodegenerative disorders, cardiovascular and metabolic diseases, cancer, aging and inflammatory conditions.

By bringing together original research articles and authoritative reviews, this issue aims to highlight emerging concepts, novel methodologies and therapeutic strategies targeting mitochondrial pathways. Collectively, these contributions underscore the pivotal role of mitochondrial bioenergetics and signaling in disease and explore how restoring mitochondrial function may open new avenues for diagnosis and treatment.

Prof. Dr. Carlos Palmeira
Dr. Anabela P. Rolo
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-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

  • mitochondria
  • bioenergetics
  • oxidative phosphorylation
  • mitochondrial signaling
  • metabolism
  • reactive oxygen species (ROS)
  • mitochondrial dynamics
  • mitophagy
  • calcium signaling
  • mitochondrial DNA
  • redox homeostasis
  • cell death
  • inflammation
  • neurodegeneration
  • cancer metabolism
  • cardiometabolic diseases
  • aging
  • therapeutic targeting

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Published Papers (2 papers)

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Research

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31 pages, 2425 KB  
Article
A Mechanism-Centered Text-Mining Landscape of Mitochondrial Bioenergetics and Signaling in Disease Research
by Harun Yonar, Furkan Çağrı Beşoluk and Tuğba Melike Parlak
Int. J. Mol. Sci. 2026, 27(15), 6577; https://doi.org/10.3390/ijms27156577 - 23 Jul 2026
Viewed by 824
Abstract
Mitochondria are increasingly recognized as integrated bioenergetic and signaling hubs across disease contexts, but the rapidly expanding literature remains fragmented across mechanisms, diseases, and analytical vocabularies. This study mapped the disease-oriented literature on mitochondrial bioenergetics and signaling from 2014 to 2025 using a [...] Read more.
Mitochondria are increasingly recognized as integrated bioenergetic and signaling hubs across disease contexts, but the rapidly expanding literature remains fragmented across mechanisms, diseases, and analytical vocabularies. This study mapped the disease-oriented literature on mitochondrial bioenergetics and signaling from 2014 to 2025 using a mechanism-centered text-mining framework integrating dictionary-based annotation and topic modeling. Records retrieved from Web of Science, Scopus, and PubMed were harmonized into a final corpus of 166,462 title–abstract records. Dictionary-based annotation was used to identify disease and mitochondrial mechanism signals, followed by disease–mechanism co-occurrence, lift-based enrichment, exploratory drug/compound annotation, non-negative matrix factorization (NMF), and structural topic modeling (STM). Publication output increased approximately 2.6-fold over the study period. The literature was organized around a central mechanistic backbone involving ROS/redox biology, cell death pathways, bioenergetics/OXPHOS, mitochondrial dysfunction/homeostasis, and quality-control processes. Cancer, cardiometabolic/metabolic disease, and neurodegeneration/neurological injury were the dominant disease contexts. Enrichment analysis revealed disease-characteristic mitochondrial signatures, while NMF identified a 20-topic thematic structure and STM showed increasing emphasis on mitochondrial dysfunction, immune-inflammatory signaling, omics-based prognostic signatures, therapeutic delivery systems, and cancer progression/resistance. Overall, mitochondrial disease research is shifting toward an integrated, application-oriented framework in which mitochondria are positioned as bioenergetic, signaling, immune-regulatory, and therapeutic-response hubs. Full article
(This article belongs to the Special Issue Mitochondrial Bioenergetics and Signaling in Diseases)
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Review

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33 pages, 13688 KB  
Review
On the Edge of Benefit and Harm: Reactive Oxygen Species in Cancer
by Anna B. Nikiforova
Int. J. Mol. Sci. 2026, 27(15), 6887; https://doi.org/10.3390/ijms27156887 - 1 Aug 2026
Viewed by 476
Abstract
Reactive oxygen species (ROS) are central regulators of cancer biology and represent a double-edged target in oncology. At physiological levels, ROS support signal transduction, proliferation, differentiation, and immune responses, whereas sustained ROS imbalance promotes DNA damage, genomic instability, metabolic reprogramming, and remodeling of [...] Read more.
Reactive oxygen species (ROS) are central regulators of cancer biology and represent a double-edged target in oncology. At physiological levels, ROS support signal transduction, proliferation, differentiation, and immune responses, whereas sustained ROS imbalance promotes DNA damage, genomic instability, metabolic reprogramming, and remodeling of the tumor microenvironment, thereby contributing to tumor initiation, progression, metastasis, and therapy resistance. Conversely, because many cancer cells operate close to the limit of tolerable oxidative stress, further ROS elevation can trigger apoptosis, ferroptosis, immunogenic cell death, and other cytotoxic programs. This review summarizes the major intracellular and microenvironmental sources of ROS, the mechanisms by which redox signaling shapes malignant transformation and tumor adaptation, and the antioxidant systems that buffer oxidative stress in cancer cells. We further discuss current therapeutic approaches based on both ROS suppression and ROS amplification, including redox-modulating small molecules, radiotherapy, photodynamic and sonodynamic therapy, catalytic nanomaterials, and ROS-responsive prodrugs and drug delivery systems. Particular attention is given to the context-dependent effects of ROS, the antioxidant paradox, tumor heterogeneity, hypoxia, off-target toxicity, and the need for robust redox biomarkers. A deeper understanding of tumor-specific redox vulnerabilities will be essential for developing precise and clinically effective ROS-oriented cancer therapies. Full article
(This article belongs to the Special Issue Mitochondrial Bioenergetics and Signaling in Diseases)
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