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Targeting Mitochondria in Aging and Disease 2.0

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: closed (30 September 2022) | Viewed by 13616

Special Issue Editors

Instituto de Investigaciones Biomédicas Alberto Sols (IIBm), CSIC-UAM, Madrid, Spain
Interests: mitochondria; metabolic diseases; oxidative stress; cardiovascular diseases; retinopathy; NAFLD; cancer; biomarkers; type 2 diabetes
Special Issues, Collections and Topics in MDPI journals
1. Department of Biomedical Sciences for Health, University of Milan, Via Mangiagalli 31, 20133 Milan, Italy
2. UO Laboratorio di Morfologia Umana Applicata, IRCCS San Donato, 20133 Milan, Italy
Interests: translational preclinical models of diseases; metabolic diseases; oxidative damage; endoplasmic reticulum stress; mitochondria; autophagy; mitophagy; role of antioxidants; ageing; sirtuins; natural compounds to limit metabolic diseases; cardiovascular damage and sirtuins modulation; obesity and mitochondrial endoplasmic reticulum interplay; selective autophagy in aging and disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Emerging evidence indicates that mitochondria, the essential energy powerhouse in cells, can be pharmacologically targeted. Aging dramatically impacts mitochondrial efficacy and plasticity, and to sustain mitochondrial biogenesis is the main objective of anti-aging medicine. Mitochondrial dysfunction at an ultrastructural level can be evidenced by the observation of abnormal cristae at the cellular level, characterized by altered size, number, and sub-cellular localization, as well as by reduced turnover and dynamics. These changes are associated with the disrupted function of the electron transport chain, showing lower electronic capacity, reduced membrane potential, increased production of superoxide, and reduced capacity to couple electronic flux to ATP synthesis. Neurons, skeletal and cardiac myocytes, and hepatocytes are among the most affected cell types due to their reliance on mitochondrial ATP output. Noted bioenergetic alterations—characteristics of aging— are also shared by cancer cells and have been suggested to have an impact on the control of cell death pathways, autophagy, and proteostasis. Recently, mitophagy has become a focus of attention in aging, metabolic diseases, and cancer. This is a selective mitochondrial clearing mechanism dependent on lysosomes, which has been shown to be defective or functionally altered, leading to the accumulation of dysfunctional mitochondria in the cell. Thus, targeting the mitochondria and restoring proper mitochondrial homeostasis are fundamental to treating disorders in which mitochondrial dysfunction has been shown to be a key driver of the disease. Novel developments have boosted our capacity to analyze mitochondria by evaluating cellular and circulating mtDNA—free and associated with regulatory factors. Therefore, the evaluation of epigenetic cues and mitochondrial medicine are challenging topics for future diagnostic and therapeutic developments. We believe that now is the time to support the exchange of ideas and the latest results on mitochondrial biology and medicine and have therefore decided to propose this Special Issue for interested clinical, academic, or industrial researchers all over the world. Original articles, comprehensive reviews, or perspective articles are welcome.

Topics of interest include, but are not limited to, the following:

  • Mitochondria in aging;
  • Mitochondria in exercise;
  • Mitochondria in cancer,
  • Mitochondria in neurodegeneration;
  • Mitochondria in metabolic diseases;
  • Mitochondrial mtDNA regulation;
  • Mitochondrial oxidative pathways;
  • Hypoxia regulation;

Antioxidants and nutraceutical drugs.

Dr. Maria Monsalve
Dr. Alessandra Stacchiotti
Guest Editors

Manuscript Submission Information

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Keywords

  • mitophagy
  • new generation antioxidants
  • exercise
  • aging
  • metabolic diseases
  • neurodegenerative diseases
  • mitochondrial plasticity
  • targeting mitochondria
  • epigenetics
  • mtDNA
  • cancer

Related Special Issue

Published Papers (4 papers)

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Research

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13 pages, 2841 KiB  
Article
Galangin Rescues Alzheimer’s Amyloid-β Induced Mitophagy and Brain Organoid Growth Impairment
by Ru Zhang, Juan Lu, Gang Pei and Shichao Huang
Int. J. Mol. Sci. 2023, 24(4), 3398; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24043398 - 08 Feb 2023
Cited by 2 | Viewed by 1800
Abstract
Dysfunctional mitochondria and mitophagy are hallmarks of Alzheimer’s disease (AD). It is widely accepted that restoration of mitophagy helps to maintain cellular homeostasis and ameliorates the pathogenesis of AD. It is imperative to create appropriate preclinical models to study the role of mitophagy [...] Read more.
Dysfunctional mitochondria and mitophagy are hallmarks of Alzheimer’s disease (AD). It is widely accepted that restoration of mitophagy helps to maintain cellular homeostasis and ameliorates the pathogenesis of AD. It is imperative to create appropriate preclinical models to study the role of mitophagy in AD and to assess potential mitophagy-targeting therapies. Here, by using a novel 3D human brain organoid culturing system, we found that amyloid-β (Aβ1-42,10 μM) decreased the growth level of organoids, indicating that the neurogenesis of organoids may be impaired. Moreover, Aβ treatment inhibited neural progenitor cell (NPC) growth and induced mitochondrial dysfunction. Further analysis revealed that mitophagy levels were reduced in the brain organoids and NPCs. Notably, galangin (10 μM) treatment restored mitophagy and organoid growth, which was inhibited by Aβ. The effect of galangin was blocked by the mitophagy inhibitor, suggesting that galangin possibly acted as a mitophagy enhancer to ameliorate Aβ-induced pathology. Together, these results supported the important role of mitophagy in AD pathogenesis and suggested that galangin may be used as a novel mitophagy enhancer to treat AD. Full article
(This article belongs to the Special Issue Targeting Mitochondria in Aging and Disease 2.0)
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Review

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11 pages, 882 KiB  
Review
Significance of Mitochondrial Dysfunction in the Progression of Multiple Sclerosis
by Alexander V. Blagov, Vasily N. Sukhorukov, Alexander N. Orekhov, Margarita A. Sazonova and Alexandra A. Melnichenko
Int. J. Mol. Sci. 2022, 23(21), 12725; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232112725 - 22 Oct 2022
Cited by 7 | Viewed by 1884
Abstract
The prevalence of multiple sclerosis and the complexity of its etiology and pathogenesis require further study of the factors underlying the progression of this disease. The prominent role of mitochondria in neurons makes this organelle a vulnerable target for CNS diseases. The purpose [...] Read more.
The prevalence of multiple sclerosis and the complexity of its etiology and pathogenesis require further study of the factors underlying the progression of this disease. The prominent role of mitochondria in neurons makes this organelle a vulnerable target for CNS diseases. The purpose of this review is to consider the role of mitochondrial dysfunction in the pathogenesis of multiple sclerosis, as well as to propose new promising therapeutic strategies aimed at restoring mitochondrial function in multiple sclerosis. Full article
(This article belongs to the Special Issue Targeting Mitochondria in Aging and Disease 2.0)
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14 pages, 329 KiB  
Review
Mitochondrial Dysfunction and Neurodegenerative Disorders: Role of Nutritional Supplementation
by David Mantle and Iain Parry Hargreaves
Int. J. Mol. Sci. 2022, 23(20), 12603; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232012603 - 20 Oct 2022
Cited by 14 | Viewed by 4112
Abstract
Mitochondrial dysfunction has been implicated in the pathogenesis of a number of neurodegenerative disorders, including Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis, multisystem atrophy, and progressive supranuclear palsy. This article is concerned specifically with mitochondrial dysfunction as defined by reduced capacity for ATP [...] Read more.
Mitochondrial dysfunction has been implicated in the pathogenesis of a number of neurodegenerative disorders, including Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis, multisystem atrophy, and progressive supranuclear palsy. This article is concerned specifically with mitochondrial dysfunction as defined by reduced capacity for ATP production, the role of depleted levels of key nutritionally related metabolites, and the potential benefit of supplementation with specific nutrients of relevance to normal mitochondrial function in the above neurodegenerative disorders. The article provides a rationale for a combination of CoQ10, B-vitamins/NADH, L-carnitine, vitamin D, and alpha-lipoic acid for the treatment of the above neurodegenerative disorders. Full article
(This article belongs to the Special Issue Targeting Mitochondria in Aging and Disease 2.0)
14 pages, 1772 KiB  
Review
MOTS-c, the Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases
by Zahra Mohtashami, Mithalesh K. Singh, Nasim Salimiaghdam, Mustafa Ozgul and M. Cristina Kenney
Int. J. Mol. Sci. 2022, 23(19), 11991; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911991 - 09 Oct 2022
Cited by 11 | Viewed by 5170
Abstract
MOTS-c, a 16 amino acid mitochondrial derived peptide, is encoded from the 12S rRNA region of the mitochondrial genome. Under stress conditions, MOTS-c translocates to the nucleus where it regulates a wide range of genes in response to metabolic dysfunction. It is colocalized [...] Read more.
MOTS-c, a 16 amino acid mitochondrial derived peptide, is encoded from the 12S rRNA region of the mitochondrial genome. Under stress conditions, MOTS-c translocates to the nucleus where it regulates a wide range of genes in response to metabolic dysfunction. It is colocalized to mitochondria in various tissues and is found in plasma, but the levels decline with age. Since MOTS-c has important cellular functions as well as a possible hormonal role, it has been shown to have beneficial effects on age-related diseases including Diabetes, Cardiovascular diseases, Osteoporosis, postmenopausal obesity and Alzheimer. Aging is characterized by gradual loss of (mitochondrial) metabolic balance, decreased muscle homeostasis and eventual diminished physical capability, which potentially can be reversed with MOTS-c treatment. This review examines the latest findings on biological effects of MOTS-c as a nuclear regulatory peptide and focuses on the role of MOTS-c in aging and age-related disorders, including mechanisms of action and therapeutic potential. Full article
(This article belongs to the Special Issue Targeting Mitochondria in Aging and Disease 2.0)
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