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Mitochondrial Function in Health and Diseases
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Mitochondrial Function in Health and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 2525

Special Issue Editor

Dr. Sally P. Wheatley

E-Mail Website
Guest Editor
School of Life Sciences, University of Nottingham, Nottingham NG7 2UH, UK
Interests: cancer; mitochondria; survivin; autophagy; apoptosis

Special Issue Information

Dear Colleagues,

Mitochondria are vital to eukaryotic life. These maternally inherited organelles are highly dynamic, have their own genome, reproduce by fission and subsequent biogenesis, are repaired via fusion, and are destroyed through a specialised form of autophagy called “mitophagy”. Dubbed as the “power houses of the cell”, they produce ATP via oxidative phosphorylation for cellular energetics. They are also the first responders to stress and the principal organelles responsible for inducing intrinsic apoptosis to eliminate defective cells, to prevent diseases such as cancers. Somewhat usurped by these key roles in health and disease, their lesser known functions include, but are not limited to, the maintenance of iron levels, calcium regulation, and lipid production, which are also critical to life. This Special Issue will bring together a collection of novel research articles that highlight the molecular mechanisms underlying the many functions of these fascinating and fundamental organelles on which all eukaryotes depend.

Dr. Sally P. Wheatley
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 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

  • mitochondria
  • metabolism
  • lipid
  • ATP
  • respiration
  • calcium
  • iron, inheritance
  • apoptosis

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Published Papers (4 papers)

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Research

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28 pages, 2614 KiB  
Article
Combination of Low-Dose Sulforaphane and Docetaxel on Mitochondrial Function and Metabolic Reprogramming in Prostate Cancer Cell Lines
by Ana Peñata-Taborda, Pedro Espitia-Pérez, Lyda Espitia-Pérez, Andrés Coneo-Pretelt, Hugo Brango, Dina Ricardo-Caldera, Gean Arteaga-Arroyo, Luisa Jiménez-Vidal, Claudia Galeano-Páez, Karina Pastor-Sierra, Alicia Humanez-Alvarez, Osnamir Bru-Cordero, Nathalia Jones-Cifuentes, Bladimiro Rincón-Orozco, Stelia Mendez-Sanchez and Mario Negrette-Guzmán
Int. J. Mol. Sci. 2025, 26(3), 1013; https://doi.org/10.3390/ijms26031013 - 24 Jan 2025
Viewed by 670
Abstract
Considering the limitations of monotherapies due to chemoresistance and side effects, this research aimed to determine whether low doses of sulforaphane (SFN) combined with docetaxel (DCT) could enhance therapeutic efficacy. Prostate cancer cell lines LNCaP and PC-3 were treated with individual IC50 doses [...] Read more.
Considering the limitations of monotherapies due to chemoresistance and side effects, this research aimed to determine whether low doses of sulforaphane (SFN) combined with docetaxel (DCT) could enhance therapeutic efficacy. Prostate cancer cell lines LNCaP and PC-3 were treated with individual IC50 doses of SFN and DCT and half-reduced IC50 values for the SFN:DCT combination. Metabolic markers, including glucose consumption, lactate production, reactive oxygen species (ROS), mitochondrial mass, and caspase activity, were assessed. In LNCaP cells, the SFN:DCT combination reduced cell viability to 50%, comparable to DCT monotherapy (48%). Caspase 3 activation was also higher with SFN:DCT (2.4 ± 0.75 RFU) than DCT alone (2.1 ± 0.47 RFU), while caspase 8 activation remained comparable, indicating equivalent effectiveness at lower concentrations. In PC-3 cells, the combination induced caspase 3 activation (1.16 ± 0.0484 RFU) at levels slightly lower than DCT (1.51 ± 0.2062 RFU) but achieved greater reductions in mitochondrial mass, reflecting its ability to target metabolic vulnerabilities in aggressive phenotypes. Our findings suggest that the SFN:DCT combination is a promising strategy for early-stage prostate cancer. By achieving comparable efficacy to DCT monotherapy at low doses, the SFN:DCT combination maintains the therapeutic impact, mitigating the adverse effects of conventional DCT treatment. Full article
(This article belongs to the Special Issue Mitochondrial Function in Health and Diseases)
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24 pages, 3729 KiB  
Article
Time Course of Mitochondrial Antioxidant Markers in a Preclinical Model of Severe Penetrating Traumatic Brain Injury
by Sudeep Musyaju, Hiren R. Modi, Deborah A. Shear, Anke H. Scultetus and Jignesh D. Pandya
Int. J. Mol. Sci. 2025, 26(3), 906; https://doi.org/10.3390/ijms26030906 - 22 Jan 2025
Viewed by 434
Abstract
Traumatic brain injury (TBI) results from external mechanical forces exerted on the brain, triggering secondary injuries due to cellular excitotoxicity. A key indicator of damage is mitochondrial dysfunction, which is associated with elevated free radicals and disrupted redox balance following TBI. However, the [...] Read more.
Traumatic brain injury (TBI) results from external mechanical forces exerted on the brain, triggering secondary injuries due to cellular excitotoxicity. A key indicator of damage is mitochondrial dysfunction, which is associated with elevated free radicals and disrupted redox balance following TBI. However, the temporal changes in mitochondrial redox homeostasis after penetrating TBI (PTBI) have not been thoroughly examined. This study aimed to investigate redox alterations from 30 min to two-weeks post-injury in adult male Sprague Dawley rats that experienced either PTBI or a Sham craniectomy. Redox parameters were measured at several points: 30 min, 3 h, 6 h, 24 h, 3 d, 7 d, and 14 d post-injury. Mitochondrial samples from the injury core and perilesional areas exhibited significant elevations in protein modifications including 3-nitrotyrosine (3-NT) and protein carbonyl (PC) adducts (14–53%, vs. Sham). In parallel, antioxidants such as glutathione, NADPH, peroxiredoxin-3 (PRX-3), thioredoxin-2 (TRX-2), and superoxide dismutase 2 (SOD2) were significantly depleted (20–80%, vs. Sham). In contrast, catalase (CAT) expression showed a significant increase (45–75%, vs. Sham). These findings indicate a notable imbalance in redox parameters over the two-week post-PTBI period suggesting that the therapeutic window to employ antioxidant therapy extends well beyond 24 h post-TBI. Full article
(This article belongs to the Special Issue Mitochondrial Function in Health and Diseases)
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18 pages, 5240 KiB  
Article
Assessing the Efficacy of Mitochondria-Accumulating Self-Assembly Peptides in Pancreatic Cancer: An Animal Study
by Ho Joong Choi, Seongeon Jin, Junghyun Park, Dosang Lee, Hee Jeong Jeong, Ok-Hee Kim, Ja-Hyoung Ryu and Say-June Kim
Int. J. Mol. Sci. 2025, 26(2), 784; https://doi.org/10.3390/ijms26020784 - 17 Jan 2025
Viewed by 494
Abstract
Although pancreatic cancer presents with one of the most unfavorable prognoses, its treatment options are very limited. Mitochondria-targeting moieties, considered a new and prominent treatment modality, are expected to demonstrate synergistic anticancer effects due to their distinct mechanism compared to conventional chemotherapeutic approaches. [...] Read more.
Although pancreatic cancer presents with one of the most unfavorable prognoses, its treatment options are very limited. Mitochondria-targeting moieties, considered a new and prominent treatment modality, are expected to demonstrate synergistic anticancer effects due to their distinct mechanism compared to conventional chemotherapeutic approaches. This study evaluated the therapeutic potential of mitochondria-accumulating self-assembly peptides, referred to as Mito-FFs, utilizing both in vitro and in vivo pancreatic cancer models. Cellular viability assays revealed a concentration-dependent decrease in the survival of MIA-PACA2 pancreatic cancer cells upon exposure to Mito-FF treatment (p < 0.05). Subsequent in vitro Mito-FF treatments prompted the use of several molecular analyses, including Real-time PCR, Western blot analysis, and MitoSOX staining, which collectively indicated an upsurge in apoptosis, a concurrent reduction in the antioxidant enzyme expression, and an elevation in mitochondrial ROS levels (p < 0.05). In a murine xenograft model of pancreatic cancer, the intravenous administration of Mito-FF yielded a notable reduction in the tumor volume. Moreover, it upregulated the expression of pro-apoptotic markers, such as cleaved PARP and c-caspase 3, while concurrently downregulating the expression of an anti-apoptotic marker, MCL-1, as evidenced by both Western blot analysis and immunohistochemical staining (p < 0.05). It also resulted in the reduced expression of antioxidant enzymes like HO-1, catalase, and SOD2 within excised tumor tissues, as confirmed using Western blot analysis (p < 0.05). Cumulatively, the findings underscore the significant anticancer efficacy of Mito-FF against pancreatic cancer cells, predominantly mediated through the induction of apoptosis, suppression of antioxidant enzyme expression, and enhancement of mitochondrial ROS levels within the tumor microenvironment. Full article
(This article belongs to the Special Issue Mitochondrial Function in Health and Diseases)
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Review

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19 pages, 1528 KiB  
Review
A Comprehensive Review of the Contribution of Mitochondrial DNA Mutations and Dysfunction in Polycystic Ovary Syndrome, Supported by Secondary Database Analysis
by Hiroshi Kobayashi, Sho Matsubara, Chiharu Yoshimoto, Hiroshi Shigetomi and Shogo Imanaka
Int. J. Mol. Sci. 2025, 26(3), 1172; https://doi.org/10.3390/ijms26031172 - 29 Jan 2025
Viewed by 375
Abstract
Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting women of reproductive age characterized by a spectrum of clinical, metabolic, reproductive, and psychological abnormalities. This syndrome is associated with significant long-term health risks, necessitating elucidation of its pathophysiology, early diagnosis, and comprehensive [...] Read more.
Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting women of reproductive age characterized by a spectrum of clinical, metabolic, reproductive, and psychological abnormalities. This syndrome is associated with significant long-term health risks, necessitating elucidation of its pathophysiology, early diagnosis, and comprehensive management strategies. Several contributory factors in PCOS, including androgen excess and insulin resistance, collectively enhance oxidative stress, which subsequently leads to mitochondrial dysfunction. However, the precise mechanisms through which oxidative stress induces mitochondrial dysfunction remain incompletely understood. Comprehensive searches of electronic databases were conducted to identify relevant studies published up to 30 September 2024. Mitochondria, the primary sites of reactive oxygen species (ROS) generation, play critical roles in energy metabolism and cellular homeostasis. Oxidative stress can inflict damage on components, including lipids, proteins, and DNA. Damage to mitochondrial DNA (mtDNA), which lacks efficient repair mechanisms, may result in mutations that impair mitochondrial function. Dysfunctional mitochondrial activity further amplifies ROS production, thereby perpetuating oxidative stress. These disruptions are implicated in the complications associated with the syndrome. Advances in genetic analysis technologies, including next-generation sequencing, have identified point mutations and deletions in mtDNA, drawing significant attention to their association with oxidative stress. Emerging data from mtDNA mutation analyses challenge conventional paradigms and provide new insights into the role of oxidative stress in mitochondrial dysfunction. We are rethinking the pathogenesis of PCOS based on these database analyses. In conclusion, this review explores the intricate relationship between oxidative stress, mtDNA mutations, and mitochondrial dysfunction, offers an updated perspective on the pathophysiology of PCOS, and outlines directions for future research. Full article
(This article belongs to the Special Issue Mitochondrial Function in Health and Diseases)
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