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Mitochondria as a Key Organelle for Novel Treatments Targeting Metabolic...
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Mitochondria as a Key Organelle for Novel Treatments Targeting Metabolic Diseases and Aging

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (15 January 2022) | Viewed by 10661

Special Issue Editor

Dr. João S. Teodoro

E-Mail Website
Guest Editor
Departamento de Ciências da Vida da Universidade de Coimbra, Centro De Neurociências e Biologia Celular, 3004-504 Coimbra, Portugal
Interests: mitochondrial bioenergetics; obesity and type 2 diabetes; mitochondrial dynamics; bile acids’ metabolic effects; nanotoxicology

Special Issue Information

Dear Colleagues,

It is my great pleasure to invite your expert contributions to this Special Issue focused on the topic of novel therapeutics that target mitochondrial function for the treatment and prevention of metabolic diseases and aging. Mitochondrial function is paramount to the homeostasis of metabolism and cellular function. In fact, most metabolic diseases are rooted in mitochondrial dysfunction, either as involved organelles or as the originator of the cellular dysfunction. Over the years, various therapeutic strategies have targeted the maintenance of mitochondrial function. While most have shown promising results in the laboratory, the transition to the bedside has been slow and mostly inefficient. As such, new compounds, interventions or combined strategies are required to achieve the ubiquitously desired outcomes.

This Special Issue aims to publish various reports and perspectives on the matter, stirring interest for novel players in mitochondria, or fresh looks into tested targets. It is my firm belief that these new strategies and treatments will bring forth the potential albeit elusive treatments for metabolic diseases such as obesity, type 2 diabetes, and cardiovascular dysfunction, which are in themselves indelibly associated with the multifactorial process of cellular aging and organ loss of function.

Dr. João S. Teodoro
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. Biomolecules 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 2700 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

  • mitochondrial bioenergetics
  • metabolism
  • aging
  • new therapeutics

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Published Papers (2 papers)

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Research

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28 pages, 3457 KiB  
Article
Cytotoxicity and Mitochondrial Effects of Phenolic and Quinone-Based Mitochondria-Targeted and Untargeted Antioxidants on Human Neuronal and Hepatic Cell Lines: A Comparative Analysis
by Carlos Fernandes, Afonso J. C. Videira, Caroline D. Veloso, Sofia Benfeito, Pedro Soares, João D. Martins, Beatriz Gonçalves, José F. S. Duarte, António M. S. Santos, Paulo J. Oliveira, Fernanda Borges, José Teixeira and Filomena S. G. Silva
Biomolecules 2021, 11(11), 1605; https://doi.org/10.3390/biom11111605 - 29 Oct 2021
Cited by 7 | Viewed by 3021
Abstract
Mitochondriotropic antioxidants (MC3, MC6.2, MC4 and MC7.2) based on dietary antioxidants and analogs (caffeic, hydrocaffeic, trihydroxyphenylpropanoic and trihydroxycinnamic acids) were developed. In this study, we evaluate and compare the cytotoxicity profile of novel mitochondria-targeted molecules (generally [...] Read more.
Mitochondriotropic antioxidants (MC3, MC6.2, MC4 and MC7.2) based on dietary antioxidants and analogs (caffeic, hydrocaffeic, trihydroxyphenylpropanoic and trihydroxycinnamic acids) were developed. In this study, we evaluate and compare the cytotoxicity profile of novel mitochondria-targeted molecules (generally known as MitoCINs) on human HepG2 and differentiated SH-SY5Y cells with the quinone-based mitochondria-targeted antioxidants MitoQ and SkQ1 and with two non-targeted antioxidants, resveratrol and coenzyme Q10 (CoQ10). We further evaluate their effects on mitochondrial membrane potential, cellular oxygen consumption and extracellular acidification rates. Overall, MitoCINs derivatives reduced cell viability at concentrations about six times higher than those observed with MitoQ and SkQ1. A toxicity ranking for both cell lines was produced: MC4 < MC7.2 < MC3 < MC6.2. These results suggest that C-6 carbon linker and the presence of a pyrogallol group result in lower cytotoxicity. MC3 and MC6.2 affected the mitochondrial function more significantly relative to MitoQ, SkQ1, resveratrol and CoQ10, while MC4 and MC7.2 displayed around 100–1000 times less cytotoxicity than SkQ1 and MitoQ. Based on the mitochondrial and cytotoxicity cellular data, MC4 and MC7.2 are proposed as leads that can be optimized to develop safe drug candidates with therapeutic application in mitochondrial oxidative stress-related diseases. Full article
(This article belongs to the Special Issue Mitochondria as a Key Organelle for Novel Treatments Targeting Metabolic Diseases and Aging)
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Review

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29 pages, 1310 KiB  
Review
Nuclear-Mitochondrial Interactions
by Brittni R. Walker and Carlos T. Moraes
Biomolecules 2022, 12(3), 427; https://doi.org/10.3390/biom12030427 - 10 Mar 2022
Cited by 50 | Viewed by 6970
Abstract
Mitochondria, the cell’s major energy producers, also act as signaling hubs, interacting with other organelles both directly and indirectly. Despite having its own circular genome, the majority of mitochondrial proteins are encoded by nuclear DNA. To respond to changes in cell physiology, the [...] Read more.
Mitochondria, the cell’s major energy producers, also act as signaling hubs, interacting with other organelles both directly and indirectly. Despite having its own circular genome, the majority of mitochondrial proteins are encoded by nuclear DNA. To respond to changes in cell physiology, the mitochondria must send signals to the nucleus, which can, in turn, upregulate gene expression to alter metabolism or initiate a stress response. This is known as retrograde signaling. A variety of stimuli and pathways fall under the retrograde signaling umbrella. Mitochondrial dysfunction has already been shown to have severe implications for human health. Disruption of retrograde signaling, whether directly associated with mitochondrial dysfunction or cellular environmental changes, may also contribute to pathological deficits. In this review, we discuss known signaling pathways between the mitochondria and the nucleus, examine the possibility of direct contacts, and identify pathological consequences of an altered relationship. Full article
(This article belongs to the Special Issue Mitochondria as a Key Organelle for Novel Treatments Targeting Metabolic Diseases and Aging)
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