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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
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
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 (1 paper)

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Review

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 3
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)
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