Dear Colleagues,

We are leading the following Special Issue entitled “Antioxidants in Mitochondrial Dysfunction Disease” in the journal Antioxidants.

Mitochondria act as master regulators inside our cell. While influencing the intracellular availability of high-energy molecules, such as adenosine-5′-triphosphate (ATP), their status orchestrates the function of almost every biochemical and signaling process, either directly or indirectly.  It is thus not surprising that mitochondrial dysfunctions are a common signature of a plethora of different acute and chronic conditions spanning from musculoskeletal diseases (cardiovascular diseases, fibromyalgia, chronic fatigue, skeletal muscle atrophy) to metabolic syndromes (type II diabetes hypercholesterolemia, hypertriglyceridemia) and evolving in the most different symptoms, from alopecia to infertility.

Both preclinical and clinical evidence has shown antioxidants ameliorating the quality of life of people affected by mitochondrial diseases. Endogenous antioxidants (Glutathione, α-lipoic acid), vitamins (mostly C, D, E, thiamine, and riboflavin), metabolites (NADH, coenzyme Q10), minerals (magnesium, calcium, phosphate), as well as exogenous antioxidants such as stilbenes and polyphenols (Resveratrol, Procyanidins, Catechins) or sources of unsaturated fatty acids like fish or seed oils (Sesame, Quinoa) all seem to partially rescue mitochondrial defects.

Antioxidants are supposed to act by clearing out cells and biological fluids from harmful reactive oxygen species (ROS), reactive nitrogen species (RNS) and pro-oxidant molecules such as trimethylamine oxide (TMAO). However, some of them have been shown to directly promote oxidative phosphorylation and mitochondrial ATP production, fostering electron transport along the inner mitochondrial membrane as well as H+-pump activity. Some others indirectly affect mitochondrial activity by promoting the catabolic reactions (fatty acid β-oxidation, glutamine conversion to alpha-ketoglutarate, Krebs cycle) necessary to fulfill mitochondrial requirements for intermediates.

Contributions to this Special Issue may cover all research aspects related to endogenous and exogenous antioxidants endowed with either direct or indirect mitochondrial promoting activity. Preclinical and clinical studies are welcome as well as in vitro studies describing either conventional or non-canonical mechanisms underpinning antioxidants’ health-promoting activity.

Prof. Mariano Stornaiuolo
Prof. Ettore Novellino
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 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.

• Mitochondria
• Endogenous antioxidants
• Plant antioxidants
• ROS
• RNS
• TMAO
• Musculoskeletal disease
• Metabolic syndrome
• CVD