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Antioxidants
Special Issues
CoQ10 and Aging and Age-Related Diseases—2nd Edition
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CoQ10 and Aging and Age-Related Diseases—2nd Edition

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Antioxidant Enzyme Systems".

Deadline for manuscript submissions: 30 October 2024 | Viewed by 4631

Special Issue Editor

Dr. Guillermo López Lluch

E-Mail Website1 Website2
Guest Editor
Department of Physiology, Anatomy and Cell Biology, Andalusian Centre of Developmental Biology, Universidad Pablo de Olavide, 41013 Seville, Spain
Interests: aging; metabolism; antioxidants; calorie restriction; physical activity; exercise; neurodegeneration; muscle; liver; immunology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Coenzyme Q10 is a molecule essential for life in all organisms. Its function is key in many activities of mitochondria, since it transfers electrons from complexes I and II and other oxidoreductases, such as dihydroorotate dehydrogenase and mitochondrial GAPDH, to complex III. This makes CoQ10 essential for producing energy in mitochondria and also for the synthesis of intermediaries in the synthesis of nucleotides as well as in many other cell functions in which mitochondria are involved.

Further, CoQ10 is a key lipidic antioxidant preventing the oxidation of lipids in cell membranes and also in lipoproteins in plasma. This key function makes CoQ10 essential for the prevention of ferroptosis and other dysfunctions associated with lipid peroxidation, including inflammation. This makes CoQ10 an essential factor involved in different aspects related to aging and age-related diseases such as cardiovascular and neurological diseases, kidney dysfunction, muscle wasting, immunological dysfunction and inflammatory processes, among others. 

We invite you to submit your latest original research findings or review articles to this Special Issue. In this Special Issue, we want to summarize and increase knowledge of the important function of CoQ10 in aging and its relationship with age-related diseases, with a focus on the antioxidant function of CoQ10 in the prevention of oxidative damage in cell membranes and in the regulation of CoQ10-dependent activities. Its relationship with nutrition, life habits, and health during aging will be another important aspect to be highlighted in this Special Issue.

Further, studies of the importance of the bioavailability of this molecule in elderly people and/or the induction of its synthesis during aging are very welcome since these aspects have not currently been completely addressed.

I look forward to receiving your contribution.

Dr. Guillermo López Lluch
Guest Editor

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. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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
  • age-related diseases
  • CoQ10
  • antioxidant
  • mitochondria
  • plasma membrane
  • metabolism

Published Papers (2 papers)

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Research

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14 pages, 4416 KiB  
Article
Spatial and Temporal Protein Modules Signatures Associated with Alzheimer Disease in 3xTg-AD Mice Are Restored by Early Ubiquinol Supplementation
by Emilio Llanos-González, Francisco J. Sancho-Bielsa, Javier Frontiñán-Rubio, Yoana Rabanal-Ruíz, Sonia García-Carpintero, Eduardo Chicano, Isabel Úbeda-Banon, Alicia Flores-Cuadrado, Lydia Giménez-Llort, Francisco Javier Alcaín, Juan Ramón Peinado and Mario Durán-Prado
Antioxidants 2023, 12(3), 747; https://doi.org/10.3390/antiox12030747 - 19 Mar 2023
Cited by 2 | Viewed by 2217
Abstract
Despite its robust proteopathic nature, the spatiotemporal signature of disrupted protein modules in sporadic Alzheimer’s disease (AD) brains remains poorly understood. This considered oxidative stress contributes to AD progression and early intervention with coenzyme Q10 or its reduced form, ubiquinol, delays the progression [...] Read more.
Despite its robust proteopathic nature, the spatiotemporal signature of disrupted protein modules in sporadic Alzheimer’s disease (AD) brains remains poorly understood. This considered oxidative stress contributes to AD progression and early intervention with coenzyme Q10 or its reduced form, ubiquinol, delays the progression of the disease. Using MALDI–MSI and functional bioinformatic analysis, we have developed a protocol to express how deregulated protein modules arise from hippocampus and cortex in the AD mice model 3xTG-AD in an age-dependent manner. This strategy allowed us to identify which modules can be efficiently restored to a non-pathological condition by early intervention with ubiquinol. Indeed, an early deregulation of proteostasis-related protein modules, oxidative stress and metabolism has been observed in the hippocampus of 6-month mice (early AD) and the mirrored in cortical regions of 12-month mice (middle/late AD). This observation has been validated by IHC using mouse and human brain sections, suggesting that these protein modules are also affected in humans. The emergence of disrupted protein modules with AD signature can be prevented by early dietary intervention with ubiquinol in the 3xTG-AD mice model. Full article
(This article belongs to the Special Issue CoQ10 and Aging and Age-Related Diseases—2nd Edition)
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Review

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21 pages, 1333 KiB  
Review
CoQ10 and Mitochondrial Dysfunction in Alzheimer’s Disease
by Zdeněk Fišar and Jana Hroudová
Antioxidants 2024, 13(2), 191; https://doi.org/10.3390/antiox13020191 - 02 Feb 2024
Viewed by 1902
Abstract
The progress in understanding the pathogenesis and treatment of Alzheimer’s disease (AD) is based on the recognition of the primary causes of the disease, which can be deduced from the knowledge of risk factors and biomarkers measurable in the early stages of the [...] Read more.
The progress in understanding the pathogenesis and treatment of Alzheimer’s disease (AD) is based on the recognition of the primary causes of the disease, which can be deduced from the knowledge of risk factors and biomarkers measurable in the early stages of the disease. Insights into the risk factors and the time course of biomarker abnormalities point to a role for the connection of amyloid beta (Aβ) pathology, tau pathology, mitochondrial dysfunction, and oxidative stress in the onset and development of AD. Coenzyme Q10 (CoQ10) is a lipid antioxidant and electron transporter in the mitochondrial electron transport system. The availability and activity of CoQ10 is crucial for proper mitochondrial function and cellular bioenergetics. Based on the mitochondrial hypothesis of AD and the hypothesis of oxidative stress, the regulation of the efficiency of the oxidative phosphorylation system by means of CoQ10 can be considered promising in restoring the mitochondrial function impaired in AD, or in preventing the onset of mitochondrial dysfunction and the development of amyloid and tau pathology in AD. This review summarizes the knowledge on the pathophysiology of AD, in which CoQ10 may play a significant role, with the aim of evaluating the perspective of the pharmacotherapy of AD with CoQ10 and its analogues. Full article
(This article belongs to the Special Issue CoQ10 and Aging and Age-Related Diseases—2nd Edition)
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