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Mitochondrial Metabolism and Metal Ions Metabolism in Human Health and Diseases

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

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 14168

Special Issue Editors

Dr. Junjie Luo

E-Mail Website
Guest Editor
Department of Nutrition and Health, Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, Beijing 100083, China
Interests: metabolic diseases; cancer; aging; molecular nutrition; mitochondrial metabolism; mitochondrial metal ions; mtDNA mutation/editing; ROS; ferroptosis
Special Issues, Collections and Topics in MDPI journals
Dr. Yongting Luo

E-Mail Website
Guest Editor
Beijing Advanced Innovation Center for Food Nutrition and Human Health, Department of Nutrition and Health, China Agricultural University, Beijing 100083, China
Interests: cardiovascular disease; atherosclerosis; vascular remodeling; mitochondria; hypertension; cell signaling; mTOR; iron metabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Peng An

E-Mail Website
Guest Editor
Beijing Advanced Innovation Center for Food Nutrition and Human Health, Department of Nutrition and Health, China Agricultural University, Beijing 100083, China
Interests: iron metabolism; oxidative stress; intervention strategies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondrial metabolism is a fundamental requirement for life. The functions of mitochondrial metabolism are multifaceted, including bioenergetics, cell metabolism, apoptosis, fatty acid β-oxidation, reactive oxygen species signaling and redox homeostasis. Unbalanced mitochondrial metabolism is tightly coupled with mitochondrial fusion/fission, biogenesis, mitochondrial respiratory chain, mitophagy and DNA mutations. Consequently, any signaling or nutrient inputs that lead to the perturbation of mitochondrial metabolism frequently result in mitochondrial metabolic disorders through distinct mechanisms. Metal ions (such as Ca, K, Na, Mg, Fe and Zn) play significant roles in the maintenance of mitochondrial metabolism. Abnormal metal ion metabolism has been linked to mitochondrial dysfunction and associated with a series of unhealthy cellular physiological states and related diseases, although the mitochondrial transport mechanisms of metal ions are not thoroughly understood. Taken together, both mitochondrial metabolism and metal ions metabolism play key roles in human health and diseases, such as cancer, metabolic disease, cardiovascular disease, and neurodegenerative disease.

Contributions to this Special Issue will further explore the fields of mitochondrial metabolism and metal ions metabolism and provide a theoretical and molecular basis for the development of new strategies for human health and the treatment of related diseases. Well-designed research articles and reviews on these related topics, especially at the molecular level, are welcome.

Dr. Junjie Luo
Dr. Yongting Luo
Dr. Peng An
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 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
  • mitochondrial dynamics
  • mitochondrial signalling
  • metal ions metabolism
  • metal ions dynamics
  • cancer
  • metabolic disease
  • cardiovascular disease
  • neurodegenerative disease

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Published Papers (4 papers)

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Research

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16 pages, 7530 KiB  
Article
Altered Mitochondrial Dynamic in Lymphoblasts and Fibroblasts Mutated for FANCA-A Gene: The Central Role of DRP1
by Nadia Bertola, Silvia Bruno, Cristina Capanni, Marta Columbaro, Andrea Nicola Mazzarello, Fabio Corsolini, Stefano Regis, Paolo Degan, Enrico Cappelli and Silvia Ravera
Int. J. Mol. Sci. 2023, 24(7), 6557; https://doi.org/10.3390/ijms24076557 - 31 Mar 2023
Cited by 2 | Viewed by 1820
Abstract
Fanconi anemia (FA) is a rare genetic disorder characterized by bone marrow failure and aplastic anemia. So far, 23 genes are involved in this pathology, and their mutations lead to a defect in DNA repair. In recent years, it has been observed that [...] Read more.
Fanconi anemia (FA) is a rare genetic disorder characterized by bone marrow failure and aplastic anemia. So far, 23 genes are involved in this pathology, and their mutations lead to a defect in DNA repair. In recent years, it has been observed that FA cells also display mitochondrial metabolism defects, causing an accumulation of intracellular lipids and oxidative damage. However, the molecular mechanisms involved in the metabolic alterations have not yet been elucidated. In this work, by using lymphoblasts and fibroblasts mutated for the FANC-A gene, oxidative phosphorylation (OxPhos) and mitochondria dynamics markers expression was analyzed. Results show that the metabolic defect does not depend on an altered expression of the proteins involved in OxPhos. However, FA cells are characterized by increased uncoupling protein UCP2 expression. FANC-A mutation is also associated with DRP1 overexpression that causes an imbalance in the mitochondrial dynamic toward fission and lower expression of Parkin and Beclin1. Treatment with P110, a specific inhibitor of DRP1, shows a partial mitochondrial function recovery and the decrement of DRP1 and UCP2 expression, suggesting a pivotal role of the mitochondrial dynamics in the etiopathology of Fanconi anemia. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Metal Ions Metabolism in Human Health and Diseases)
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21 pages, 3691 KiB  
Article
TERT Extra-Telomeric Roles: Antioxidant Activity and Mitochondrial Protection
by Jessica Marinaccio, Emanuela Micheli, Ion Udroiu, Michela Di Nottia, Rosalba Carrozzo, Nicolò Baranzini, Annalisa Grimaldi, Stefano Leone, Sandra Moreno, Maurizio Muzzi and Antonella Sgura
Int. J. Mol. Sci. 2023, 24(5), 4450; https://doi.org/10.3390/ijms24054450 - 23 Feb 2023
Cited by 15 | Viewed by 3084
Abstract
Telomerase reverse transcriptase (TERT) is the catalytic subunit of telomerase holoenzyme, which adds telomeric DNA repeats on chromosome ends to counteract telomere shortening. In addition, there is evidence of TERT non-canonical functions, among which is an antioxidant role. In order to better investigate [...] Read more.
Telomerase reverse transcriptase (TERT) is the catalytic subunit of telomerase holoenzyme, which adds telomeric DNA repeats on chromosome ends to counteract telomere shortening. In addition, there is evidence of TERT non-canonical functions, among which is an antioxidant role. In order to better investigate this role, we tested the response to X-rays and H2O2 treatment in hTERT-overexpressing human fibroblasts (HF-TERT). We observed in HF-TERT a reduced induction of reactive oxygen species and an increased expression of the proteins involved in the antioxidant defense. Therefore, we also tested a possible role of TERT inside mitochondria. We confirmed TERT mitochondrial localization, which increases after oxidative stress (OS) induced by H2O2 treatment. We next evaluated some mitochondrial markers. The basal mitochondria quantity appeared reduced in HF-TERT compared to normal fibroblasts and an additional reduction was observed after OS; nevertheless, the mitochondrial membrane potential and morphology were better conserved in HF-TERT. Our results suggest a protective function of TERT against OS, also preserving mitochondrial functionality. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Metal Ions Metabolism in Human Health and Diseases)
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14 pages, 2490 KiB  
Article
Fucoidan Protects against Doxorubicin-Induced Cardiotoxicity by Reducing Oxidative Stress and Preventing Mitochondrial Function Injury
by Yuting Ji, Dekui Jin, Jingyi Qi, Xuan Wang, Chengying Zhang, Peng An, Yongting Luo and Junjie Luo
Int. J. Mol. Sci. 2022, 23(18), 10685; https://doi.org/10.3390/ijms231810685 - 14 Sep 2022
Cited by 13 | Viewed by 2538
Abstract
Doxorubicin (DOXO) is a potent chemotherapeutic drug widely used to treat various cancers. However, its clinical application is limited due to serious adverse effects on dose-dependent cardiotoxicity. Although the underlying mechanism has not been fully clarified, DOXO-induced cardiotoxicity has been mainly attributed to [...] Read more.
Doxorubicin (DOXO) is a potent chemotherapeutic drug widely used to treat various cancers. However, its clinical application is limited due to serious adverse effects on dose-dependent cardiotoxicity. Although the underlying mechanism has not been fully clarified, DOXO-induced cardiotoxicity has been mainly attributed to the accumulation of reactive oxygen species (ROS) in cardiomyocytes. Fucoidan, as a kind of sulphated polysaccharide existing in numerous brown seaweed, has potent anti-oxidant, immune-regulatory, anti-tumor, anti-coagulate and anti-viral activities. Here, we explore the potential protective role and mechanism of fucoidan in DOXO-induced cardiotoxicity in mice. Our results show that oral fucoidan supplement exerts potent protective effects against DOXO-induced cardiotoxicity by reducing oxidative stress and preventing mitochondrial function injury. The improved effect of fucoidan on DOXO-induced cardiotoxicity was evaluated by echocardiography, cardiac myocytes size and cardiac fibrosis analysis, and the expression of genes related to cardiac dysfunction and remodeling. Fucoidan reduced the ROS content and the MDA levels but enhanced the activity of antioxidant enzymes GSH-PX and SOD in the mouse serum in a DOXO-induced cardiotoxicity model. In addition, fucoidan also increased the ATP production capacity and restored the levels of a mitochondrial respiratory chain complex in heart tissue. Collectively, this study highlights fucoidan as a potential polysaccharide for protecting against DOXO-induced cardiovascular diseases. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Metal Ions Metabolism in Human Health and Diseases)
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Review

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31 pages, 3641 KiB  
Review
Mitochondrial Energy Metabolism in the Regulation of Thermogenic Brown Fats and Human Metabolic Diseases
by Yukimasa Takeda, Yoshinori Harada, Toshikazu Yoshikawa and Ping Dai
Int. J. Mol. Sci. 2023, 24(2), 1352; https://doi.org/10.3390/ijms24021352 - 10 Jan 2023
Cited by 17 | Viewed by 5958
Abstract
Brown fats specialize in thermogenesis by increasing the utilization of circulating blood glucose and fatty acids. Emerging evidence suggests that brown adipose tissue (BAT) prevents the incidence of obesity-associated metabolic diseases and several types of cancers in humans. Mitochondrial energy metabolism in brown/beige [...] Read more.
Brown fats specialize in thermogenesis by increasing the utilization of circulating blood glucose and fatty acids. Emerging evidence suggests that brown adipose tissue (BAT) prevents the incidence of obesity-associated metabolic diseases and several types of cancers in humans. Mitochondrial energy metabolism in brown/beige adipocytes regulates both uncoupling protein 1 (UCP1)-dependent and -independent thermogenesis for cold adaptation and the utilization of excess nutrients and energy. Many studies on the quantification of human BAT indicate that mass and activity are inversely correlated with the body mass index (BMI) and visceral adiposity. Repression is caused by obesity-associated positive and negative factors that control adipocyte browning, de novo adipogenesis, mitochondrial energy metabolism, UCP1 expression and activity, and noradrenergic response. Systemic and local factors whose levels vary between lean and obese conditions include growth factors, inflammatory cytokines, neurotransmitters, and metal ions such as selenium and iron. Modulation of obesity-associated repression in human brown fats is a promising strategy to counteract obesity and related metabolic diseases through the activation of thermogenic capacity. In this review, we highlight recent advances in mitochondrial metabolism, thermogenic regulation of brown fats, and human metabolic diseases. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Metal Ions Metabolism in Human Health and Diseases)
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