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Mitochondrial Function in Human Health and Disease: 2nd Edition
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Mitochondrial Function in Human Health and Disease: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 20 July 2025 | Viewed by 8691

Special Issue Editor

Dr. Yumay Chen

E-Mail Website
Guest Editor
Department of Medicine, Division of Endocrinology, University of California, Irvine, CA 92697, USA
Interests: cell cycle checkpoint control; DNA damage and repair pathway; Nek1 protein kinase; polycystic kidney disease; AKT and mitochondrial function
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria play critical metabolic roles in fatty acid oxidation, the Krebs cycle, and oxidative phosphorylation. All of these metabolic processes result in reactive oxygen species (ROS) production. ROS are toxic to cells as they cause oxidative damage to mitochondrial lipids, DNA, and proteins. Damaged mitochondria also release high levels of Ca2+ and cytochrome C, inducing apoptosis. To control the quality and quantity of mitochondria, selective autophagy, known as mitophagy, plays an important role by eliminating damaged mitochondria. Besides causing ROS damage in mitochondria, alterations in mitochondrial function through mutations in either the mitochondrial or nuclear genome have also been found to be associated with various diseases, such as cancer, aging, metabolic disorders, etc. The first known involvement of mitochondria in cancer came from Warburg’s landmark observation that tumors produce excess lactate in the presence of oxygen, now known as the “Warburg effect”, which is a form of aerobic glycolysis. The activation of cellular signaling transduction pathways, such as the PI3’K/PTEN/Akt pathway, also plays an important role in shifting metabolism from oxidative to glycolytic phosphorylation. Now, more evidence suggests that AKT kinase activity in mitochondria is crucial for cellular defense to extrinsic insults such as ischemia reperfusion. This Special Issue elucidates various aspects of mitochondrial function in cancer, kidney disease, apoptosis, and autophagy, and further discusses the therapeutic potential of targeting mitochondria.

Dr. Yumay Chen
Guest Editor

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Keywords

  • mitochondial genesis and disease
  • mitochondrial function and aging
  • mitochondrial dysfunction and cancer
  • mitochondrial function and apoptosis
  • mitophage
  • autophage
  • mitochondrial AKT
 

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Related Special Issue

Published Papers (6 papers)

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Research

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38 pages, 8927 KiB  
Article
Fecal Microbiota Transplantation from Mice Receiving Magnetic Mitohormesis Treatment Reverses High-Fat Diet-Induced Metabolic and Osteogenic Dysfunction
by Jun Kit Craig Wong, Bharati Kadamb Patel, Yee Kit Tai, Tuan Zea Tan, Wei Wei Thwe Khine, Way Cherng Chen, Marek Kukumberg, Jianhong Ching, Lye Siang Lee, Kee Voon Chua, Tsze Yin Tan, Kwan Yu Wu, Xizhe Bai, Jan Nikolas Iversen, Kristy Purnamawati, Rufaihah Abdul Jalil, Alan Prem Kumar, Yuan Kun Lee, Shabbir M. Moochhala and Alfredo Franco-Obregón
Int. J. Mol. Sci. 2025, 26(12), 5450; https://doi.org/10.3390/ijms26125450 - 6 Jun 2025
Viewed by 1081
Abstract
This study compared the metabolic consequences of fecal microbiota transplantation (FMT) from donor mice that had been either administered pulsed electromagnetic field (PEMF) therapy or exercised to recipient mice fed a high-fat diet (HFD). Eight weeks of PEMF treatment (10 min/week) enhanced PGC-1α-associated [...] Read more.
This study compared the metabolic consequences of fecal microbiota transplantation (FMT) from donor mice that had been either administered pulsed electromagnetic field (PEMF) therapy or exercised to recipient mice fed a high-fat diet (HFD). Eight weeks of PEMF treatment (10 min/week) enhanced PGC-1α-associated mitochondrial and metabolic gene expression in white and brown adipose to a greater degree than eight weeks of exercise (30–40 min/week). FMT from PEMF-treated donor mice recapitulated these adipogenic adaptations in HFD-fed recipient mice more faithfully than FMT from exercised donors. Direct PEMF treatment altered hepatic phospholipid composition, reducing long-chain ceramides (C16:0) and increasing very long-chain ceramides (C24:0), which could be transferred to PEMF-FMT recipient mice. FMT from PEMF-treated mice was also more effective at recovering glucose tolerance than FMT from exercised mice. PEMF treatment also enhanced bone density in both donor and HFD recipient mice. The gut Firmicutes/Bacteroidetes (F/B) ratio was lowest in both the directly PEMF-exposed and PEMF-FMT recipient mouse groups, consistent with a leaner phenotype. PEMF treatment, either directly applied or via FMT, enhanced adipose thermogenesis, ceramide levels, bone density, hepatic lipids, F/B ratio, and inflammatory blood biomarkers more than exercise. PEMF therapy may represent a non-invasive and non-strenuous method to ameliorate metabolic disorders. Full article
(This article belongs to the Special Issue Mitochondrial Function in Human Health and Disease: 2nd Edition)
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22 pages, 6338 KiB  
Article
Oxidative High Mobility Group Box-1 Accelerates Mitochondrial Transfer from Mesenchymal Stem Cells to Colorectal Cancer Cells Providing Cancer Cell Stemness
by Rika Sasaki, Yi Luo, Shingo Kishi, Ruiko Ogata, Yukiko Nishiguchi, Takamitsu Sasaki, Hitoshi Ohmori, Rina Fujiwara-Tani and Hiroki Kuniyasu
Int. J. Mol. Sci. 2025, 26(3), 1192; https://doi.org/10.3390/ijms26031192 - 30 Jan 2025
Cited by 1 | Viewed by 1069
Abstract
Mitochondria are important organelles for cell metabolism and tissue survival. Their cell-to-cell transfer is important for the fate of recipient cells. Recently, bone marrow mesenchymal stem cells (BM-MSCs) have been reported to provide mitochondria to cancer cells and rescue mitochondrial dysfunction in cancer [...] Read more.
Mitochondria are important organelles for cell metabolism and tissue survival. Their cell-to-cell transfer is important for the fate of recipient cells. Recently, bone marrow mesenchymal stem cells (BM-MSCs) have been reported to provide mitochondria to cancer cells and rescue mitochondrial dysfunction in cancer cells. However, the details of the mechanism have not yet been fully elucidated. In this study, we investigated the humoral factors inducing mitochondrial transfer (MT) and the mechanisms. BM-MSCs produced MT in colorectal cancer (CRC) cells damaged by 5-fluorouracil (5-FU), but were suppressed by the anti-high mobility group box-1 (HMGB1) antibody. BM-MSCs treated with oxidized HMGB1 had increased expression of MT-associated genes, whereas reduced HMGB1 did not. Inhibition of nuclear factor–κB, a downstream factor of HMGB1 signaling, significantly decreased MT-associated gene expression. CRC cells showed increased stemness and decreased 5-FU sensitivity in correlation with MT levels. In a mouse subcutaneous tumor model of CRC, 5-FU sensitivity decreased and stemness increased by the MT from host mouse BM-MSCs. These results suggest that oxidized HMGB1 induces MTs from MSCs to CRC cells and promotes cancer cell stemness. Targeting of oxidized HMGB1 may attenuate stemness of CRCs. Full article
(This article belongs to the Special Issue Mitochondrial Function in Human Health and Disease: 2nd Edition)
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17 pages, 2909 KiB  
Article
Mass Spectrometry Analysis of Neurotransmitter Shifting during Neurogenesis and Neurodegeneration of PC12 Cells
by Yu-Ning Jao, Yu-Jen Chao, Jui-Fen Chan and Yuan-Hao Howard Hsu
Int. J. Mol. Sci. 2024, 25(19), 10399; https://doi.org/10.3390/ijms251910399 - 27 Sep 2024
Cited by 1 | Viewed by 1166
Abstract
Parkinson’s disease (PD) affects movement; however, most patients with PD also develop nonmotor symptoms, such as hyposmia, sleep disorder, and depression. Dopamine levels in the brain have a critical influence on movement control, but other neurotransmitters are also involved in the progression of [...] Read more.
Parkinson’s disease (PD) affects movement; however, most patients with PD also develop nonmotor symptoms, such as hyposmia, sleep disorder, and depression. Dopamine levels in the brain have a critical influence on movement control, but other neurotransmitters are also involved in the progression of PD. This study analyzed the fluctuation of neurotransmitters in PC12 cells during neurogenesis and neurodegeneration by performing mass spectrometry. We found that the dopaminergic metabolism pathway of PC12 cells developed vigorously during the neuron differentiation process and that the neurotransmitters were metabolized into 3-methoxytyramine, which was released from the cells. The regulation of the intracellular and extracellular concentrations of adenosine indicated that adenine nucleotides were actively utilized in neural differentiation. Moreover, we exposed the differentiated PC12 cells to rotenone, which is a suitable material for modeling PD. The cells exposed to rotenone in the early stage of differentiation exhibited stimulated serotoninergic metabolism, and the contents of the serotoninergic neurotransmitters returned to their normal levels in the late stage of differentiation. Interestingly, the nondifferentiated cells can resist the toxicant rotenone and produce normal dopaminergic metabolites. However, when differentiated neuron cells were exposed to rotenone, they were seriously damaged, leading to a failure to produce dopaminergic neurotransmitters. In the low-dosage damage process, the amino acids that functioned as dopaminergic pathway precursors could not be absorbed by the cells, and dopamine and L-dopa were secreted and unable to be reuptaken to trigger the cell damage. Full article
(This article belongs to the Special Issue Mitochondrial Function in Human Health and Disease: 2nd Edition)
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Review

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38 pages, 2728 KiB  
Review
Mitochondrial Dysfunction in Genetic and Non-Genetic Parkinson’s Disease
by Martina Lucchesi, Letizia Biso, Marco Bonaso, Biancamaria Longoni, Bianca Buchignani, Roberta Battini, Filippo Maria Santorelli, Stefano Doccini and Marco Scarselli
Int. J. Mol. Sci. 2025, 26(9), 4451; https://doi.org/10.3390/ijms26094451 - 7 May 2025
Cited by 1 | Viewed by 866
Abstract
Mitochondrial dysfunction is a hallmark of Parkinson’s disease (PD) pathogenesis, contributing to increased oxidative stress and impaired endo-lysosomal-proteasome system efficiency underlying neuronal injury. Genetic studies have identified 19 monogenic mutations—accounting for ~10% of PD cases—that affect mitochondrial function and are associated with early- [...] Read more.
Mitochondrial dysfunction is a hallmark of Parkinson’s disease (PD) pathogenesis, contributing to increased oxidative stress and impaired endo-lysosomal-proteasome system efficiency underlying neuronal injury. Genetic studies have identified 19 monogenic mutations—accounting for ~10% of PD cases—that affect mitochondrial function and are associated with early- or late-onset PD. Early-onset forms typically involve genes encoding proteins essential for mitochondrial quality control, including mitophagy and structural maintenance, while late-onset mutations impair mitochondrial dynamics, bioenergetics, and trafficking. Atypical juvenile genetic syndromes also exhibit mitochondrial abnormalities. In idiopathic PD, environmental neurotoxins such as pesticides and MPTP act as mitochondrial inhibitors, disrupting complex I activity and increasing reactive oxygen species. These converging pathways underscore mitochondria as a central node in PD pathology. This review explores the overlapping and distinct mitochondrial mechanisms in genetic and non-genetic PD, emphasizing their role in neuronal vulnerability. Targeting mitochondrial dysfunction finally offers a promising therapeutic avenue to slow or modify disease progression by intervening at a key point of neurodegenerative convergence. Full article
(This article belongs to the Special Issue Mitochondrial Function in Human Health and Disease: 2nd Edition)
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33 pages, 2994 KiB  
Review
Mitochondrial Aconitase and Its Contribution to the Pathogenesis of Neurodegenerative Diseases
by Volodymyr Padalko, Filip Posnik and Malgorzata Adamczyk
Int. J. Mol. Sci. 2024, 25(18), 9950; https://doi.org/10.3390/ijms25189950 - 15 Sep 2024
Cited by 8 | Viewed by 3099
Abstract
This survey reviews modern ideas on the structure and functions of mitochondrial and cytosolic aconitase isoenzymes in eukaryotes. Cumulative experimental evidence about mitochondrial aconitases (Aco2) as one of the main targets of reactive oxygen and nitrogen species is generalized. The important role of [...] Read more.
This survey reviews modern ideas on the structure and functions of mitochondrial and cytosolic aconitase isoenzymes in eukaryotes. Cumulative experimental evidence about mitochondrial aconitases (Aco2) as one of the main targets of reactive oxygen and nitrogen species is generalized. The important role of Aco2 in maintenance of homeostasis of the intracellular iron pool and maintenance of the mitochondrial DNA is discussed. The role of Aco2 in the pathogenesis of some neurodegenerative diseases is highlighted. Inactivation or dysfunction of Aco2 as well as mutations found in the ACO2 gene appear to be significant factors in the development and promotion of various types of neurodegenerative diseases. A restoration of efficient mitochondrial functioning as a source of energy for the cell by targeting Aco2 seems to be one of the promising therapeutic directions to minimize progressive neurodegenerative disorders. Full article
(This article belongs to the Special Issue Mitochondrial Function in Human Health and Disease: 2nd Edition)
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Other

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14 pages, 1542 KiB  
Brief Report
Brief Weekly Magnetic Field Exposure Enhances Avian Oxidative Muscle Character During Embryonic Development
by Jasmine Lye Yee Yap, Kwan Yu Wu, Yee Kit Tai, Charlene Hui Hua Fong, Neha Manazir, Anisha Praiselin Paul, Olivia Yeo and Alfredo Franco-Obregón
Int. J. Mol. Sci. 2025, 26(11), 5423; https://doi.org/10.3390/ijms26115423 - 5 Jun 2025
Viewed by 519
Abstract
Maternal metabolic dysfunction adversely influences embryonic muscle oxidative capacity and mitochondrial biogenesis, increasing the child’s long-term risks of developing obesity and metabolic syndrome in later life. This pilot study explored the mechanistic basis of embryonic muscle metabolic programming, employing non-invasive magnetic field exposures. [...] Read more.
Maternal metabolic dysfunction adversely influences embryonic muscle oxidative capacity and mitochondrial biogenesis, increasing the child’s long-term risks of developing obesity and metabolic syndrome in later life. This pilot study explored the mechanistic basis of embryonic muscle metabolic programming, employing non-invasive magnetic field exposures. Brief (10 min) exposure to low-energy (1.5 milliTesla at 50 Hertz) pulsing electromagnetic fields (PEMFs) has been shown in mammals to promote oxidative muscle development, associated with enhanced muscular mitochondriogenesis, augmented lipid metabolism, and attenuated inflammatory status. In this study, quail eggs were used as a model system to investigate the potential of analogous PEMF therapy to modulate embryonic muscle oxidative capacity independently of maternal influence. Quail eggs were administered five 10-min PEMF exposures to either upward-directed or downward-directed magnetic fields over 13 days. Embryos receiving magnetic treatment exhibited increased embryo weight, size, and survival compared to non-exposed controls. Upward exposure was associated with larger embryos, redder breast musculature, and upregulated levels of PPAR-α and PGC-1α, transcriptional regulators promoting oxidative muscle development, mitochondriogenesis, and angiogenesis, whereas downward exposure augmented collagen levels and reduced angiogenesis. Exposure to upward PEMFs may hence serve as a method to promote embryonic growth and oxidative muscle development and improve embryonic mortality. Full article
(This article belongs to the Special Issue Mitochondrial Function in Human Health and Disease: 2nd Edition)
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