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Special Issue "Mitochondrial Dysfunction in Ageing and Diseases: Partie Deux"

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

Deadline for manuscript submissions: 31 July 2021.

Special Issue Editors

Dr. Jaime M. Ross
E-Mail Website
Guest Editor
Assistant Professor, George & Anne Ryan Institute for Neuroscience, College of Pharmacy, University of Rhode Island, Kingston, Rhode Island, USA
Department of Neuroscience, BioMedicum, Karolinska Institutet, Stockholm, Sweden
Interests: mitochondrial dysfunction; metabolism; epigenetics; development; brain plasticity; models for ageing and neurodegenerative diseases and possible treatments
Dr. Giuseppe Coppotelli
E-Mail Website
Guest Editor
Research Assistant Professor, George & Anne Ryan Institute for Neuroscience, College of Pharmacy, University of Rhode Island, Kingston, Rhode Island, USA
Interests: protein homeostasis, mitochondrial dysfunction; inflammation; models for ageing and age-related diseases and treatment strategies

Special Issue Information

Dear Colleagues,

The past two decades have witnessed an explosion of knowledge regarding how mitochondrial dysfunction may translate into aging and disease phenotypes, as well as how it is modulated by genetic and lifestyle factors. Impairment of the mitochondria may be caused by mutations or deletions in nuclear or mitochondrial DNA as well as by deterioration of quality control mechanisms. Hallmarks of mitochondrial dysfunction include decreased ATP production, decreased mitochondrial membrane potential, swollen mitochondria, damaged cristae, increased oxidative stress, and decreased mitochondrial DNA copy number. In addition to energy production, mitochondria play an important role in regulating apoptosis, buffering calcium release, retrograde signaling to the nuclear genome, producing reactive oxygen species (ROS), participating in steroid synthesis, signaling to the immune system, as well as controlling the cell cycle and cell growth. Dysfunctional mitochondria have been implicated in aging and in numerous diseases, many of which are age-related, including cancers, metabolic diseases and diabetes, inflammatory conditions, neuropathy, stroke, and neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease in addition to amyotrophic lateral sclerosis. Additionally, the link between mitochondrial metabolism and the ubiquitin proteasome and autophagy–lysosome systems is continuing to emerge as a novel factor contributing to the progression of aging and several human diseases. Lifestyle factors, such as diet and exercise, as well as small molecules have shown increasing promise as possible treatments to improve energy metabolism. Emerging evidence now also links mitochondrial dysfunction as a key player in innate immunity and chronic inflammation.

Join us as we explore advancements made in the vast field of mitochondrial biology with regards to aging and diseases. This Special Issue serves as an update to a previous issue and calls for original research, mini and full reviews, and perspectives that address the progress and current standing of mitochondrial dysfunction in the following topics:

  • aging
  • dementias and neurodegenerative diseases
  • treatments to counteract mitochondrial dysfunction
  • protein homeostasis and mtDNA quality control
  • chronic inflammation and inflammatory diseases
  • cell/retrograde signaling
  • oxidative stress
  • metabolic disorders and diabetes
  • pain
  • cancer
  • stroke

Jaime M. Ross, Ph.D.
Giuseppe Coppotelli, Ph.D.
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 papers will be 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

  • aging; dementias and neurodegenerative diseases;  treatments to counteract mitochondrial dysfunction;  protein homeostasis and mtDNA quality control;  chronic inflammation and inflammatory diseases;  cell/retrograde signaling;  oxidative stress;  metabolic disorders and diabetes; pain;  cancer;  stroke

Published Papers (4 papers)

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Open AccessArticle
Adipocyte-Mineralocorticoid Receptor Alters Mitochondrial Quality Control Leading to Mitochondrial Dysfunction and Senescence of Visceral Adipose Tissue
Int. J. Mol. Sci. 2021, 22(6), 2881; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22062881 - 12 Mar 2021
Viewed by 344
Abstract
Mineralocorticoid receptor (MR) expression is increased in the adipose tissue (AT) of obese patients and animals. We previously demonstrated that adipocyte-MR overexpression in mice (Adipo-MROE mice) is associated with metabolic alterations. Moreover, we showed that MR regulates mitochondrial dysfunction and cellular senescence in [...] Read more.
Mineralocorticoid receptor (MR) expression is increased in the adipose tissue (AT) of obese patients and animals. We previously demonstrated that adipocyte-MR overexpression in mice (Adipo-MROE mice) is associated with metabolic alterations. Moreover, we showed that MR regulates mitochondrial dysfunction and cellular senescence in the visceral AT of obese db/db mice. Our hypothesis is that adipocyte-MR overactivation triggers mitochondrial dysfunction and cellular senescence, through increased mitochondrial oxidative stress (OS). Using the Adipo-MROE mice with conditional adipocyte-MR expression, we evaluated the specific effects of adipocyte-MR on global and mitochondrial OS, as well as on OS-induced damage. Mitochondrial function was assessed by high throughput respirometry. Molecular mechanisms were probed in AT focusing on mitochondrial quality control and senescence markers. Adipo-MROE mice exhibited increased mitochondrial OS and altered mitochondrial respiration, associated with reduced biogenesis and increased fission. This was associated with OS-induced DNA-damage and AT premature senescence. In conclusion, targeted adipocyte-MR overexpression leads to an imbalance in mitochondrial dynamics and regeneration, to mitochondrial dysfunction and to ageing in visceral AT. These data bring new insights into the MR-dependent AT dysfunction in obesity. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction in Ageing and Diseases: Partie Deux)
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Review

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Open AccessReview
Mitochondrial Mutations and Genetic Factors Determining NAFLD Risk
Int. J. Mol. Sci. 2021, 22(9), 4459; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094459 - 24 Apr 2021
Viewed by 416
Abstract
NAFLD (non-alcoholic fatty liver disease) is a widespread liver disease that is often linked with other life-threatening ailments (metabolic syndrome, insulin resistance, diabetes, cardiovascular disease, atherosclerosis, obesity, and others) and canprogress to more severe forms, such as NASH (non-alcoholic steatohepatitis), cirrhosis, and HCC [...] Read more.
NAFLD (non-alcoholic fatty liver disease) is a widespread liver disease that is often linked with other life-threatening ailments (metabolic syndrome, insulin resistance, diabetes, cardiovascular disease, atherosclerosis, obesity, and others) and canprogress to more severe forms, such as NASH (non-alcoholic steatohepatitis), cirrhosis, and HCC (hepatocellular carcinoma). In this review, we summarized and analyzed data about single nucleotide polymorphism sites, identified in genes related to NAFLD development and progression. Additionally, the causative role of mitochondrial mutations and mitophagy malfunctions in NAFLD is discussed. The role of mitochondria-related metabolites of the urea cycle as a new non-invasive NAFLD biomarker is discussed. While mitochondria DNA mutations and SNPs (single nucleotide polymorphisms) canbe used as effective diagnostic markers and target for treatments, age and ethnic specificity should be taken into account. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction in Ageing and Diseases: Partie Deux)
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Open AccessReview
Mitochondrial Functioning and the Relations among Health, Cognition, and Aging: Where Cell Biology Meets Cognitive Science
Int. J. Mol. Sci. 2021, 22(7), 3562; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073562 - 30 Mar 2021
Viewed by 381
Abstract
Cognitive scientists have determined that there is a set of mechanisms common to all sensory, perceptual, and cognitive abilities and correlated with age- and disease-related declines in cognition. These mechanisms also contribute to the development and functional coherence of the large-scale brain networks [...] Read more.
Cognitive scientists have determined that there is a set of mechanisms common to all sensory, perceptual, and cognitive abilities and correlated with age- and disease-related declines in cognition. These mechanisms also contribute to the development and functional coherence of the large-scale brain networks that support complex forms of cognition. At the same time, these brain and cognitive patterns are correlated with myriad health outcomes, indicating that at least some of the underlying mechanisms are common to all biological systems. Mitochondrial functions, including cellular energy production and control of oxidative stress, among others, are well situated to explain the relations among the brain, cognition, and health. Here, I provide an overview of the relations among cognitive abilities, associated brain networks, and the importance of mitochondrial energy production for their functioning. These are then linked to the relations between cognition, health, and aging. The discussion closes with implications for better integrating research in cognitive science and cell biology in the context of developing more sensitive measures of age- and disease-related declines in cognition. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction in Ageing and Diseases: Partie Deux)
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Open AccessReview
Aging-Related Disorders and Mitochondrial Dysfunction: A Critical Review for Prospect Mitoprotective Strategies Based on Mitochondrial Nutrient Mixtures
Int. J. Mol. Sci. 2020, 21(19), 7060; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21197060 - 25 Sep 2020
Cited by 5 | Viewed by 756
Abstract
A number of aging-related disorders (ARD) have been related to oxidative stress (OS) and mitochondrial dysfunction (MDF) in a well-established body of literature. Most studies focused on cardiovascular disorders (CVD), type 2 diabetes (T2D), and neurodegenerative disorders. Counteracting OS and MDF has been [...] Read more.
A number of aging-related disorders (ARD) have been related to oxidative stress (OS) and mitochondrial dysfunction (MDF) in a well-established body of literature. Most studies focused on cardiovascular disorders (CVD), type 2 diabetes (T2D), and neurodegenerative disorders. Counteracting OS and MDF has been envisaged to improve the clinical management of ARD, and major roles have been assigned to three mitochondrial cofactors, also termed mitochondrial nutrients (MNs), i.e., α-lipoic acid (ALA), Coenzyme Q10 (CoQ10), and carnitine (CARN). These cofactors exert essential–and distinct—roles in mitochondrial machineries, along with strong antioxidant properties. Clinical trials have mostly relied on the use of only one MN to ARD-affected patients as, e.g., in the case of CoQ10 in CVD, or of ALA in T2D, possibly with the addition of other antioxidants. Only a few clinical and pre-clinical studies reported on the administration of two MNs, with beneficial outcomes, while no available studies reported on the combined administration of three MNs. Based on the literature also from pre-clinical studies, the present review is to recommend the design of clinical trials based on combinations of the three MNs. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction in Ageing and Diseases: Partie Deux)

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

1. Proposed title:  Hyperhomocysteinemia, thioretinaco ozonide, and mitochondrial dysfunction

Short abstract:  The discovery of hyperhomocysteinemia as an etiological factor in arteriosclerosis and diseases of aging, including cardiovascular disease, cancer, autoimmune diseases, and neurodegenerative diseases, led to development of the theory of thioretinaco ozonide as the active site of oxidative phosphorylation in mitochondria.  Loss of thioretinaco ozonide from mitochondria is promoted by diverse pathogenic, metabolic, nutritional, cellular and molecular factors that predispose to mitochondrial dysfunction in diseases of aging.  Therapeutic strategies that prevent loss of thioretinaco ozonide from mitochondria have the potential for treatment and prevention of diseases associated with hyperhomocysteinemia.

2. Role of Redox Signaling in Sarcopenia

Abstract: Sarcopenia is a condition in which skeletal muscle reduces mass and function over age. Severe sarcopenia results in disability, decreased quality of life, and elevated risk of death, and prevails in a growing proportion of the population. The etiological mechanism of sarcopenia is not entirely known. In this review we will focus on the role of reactive oxygen species (ROS) and oxidative stress.  Major factors contributing to sarcopenia include mitochondrial dysfunction, impaired autophagy and mitophagy, dysregulation of protein turnover, disruption of AMPK signaling, inflammation, and apoptosis. We propose that change in the sensitivity of redox signaling plays a major role in the development of sarcopenia, whereby various pathways necessary for maintenance of muscle mass and function are differentially affected by ROS and oxidative stress.

3. A mitocentric view of the main bacterial and parasitic infectious diseases in the pediatric population

4. Hyperhomocysteinemia, thioretinaco ozonide, and mitochondrial dysfunction

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