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Special Issue "Molecular Research on Mitochondrial Dysfunction"

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

Deadline for manuscript submissions: 30 April 2021.

Special Issue Editors

Dr. María Eugenia Soriano

Guest Editor
Università degli Studi di Padova, Padua, Italy
Interests: mitochondria; complexomic analysis; crisate remodelling; nucleoid dynamics; mitochondrial disease
Dr. Carlo Viscomi
Website
Guest Editor
Department of Biomedical Sciences, University of Padova, Padua, Italy
Interests: mitochondrial disease; AAV; gene therapy; mitochondrial biology; mitochondrial DNA

Special Issue Information

Dear Colleagues,

It is becoming increasingly clear and widely accepted that mitochondria play a central role in human pathology, not only in relation to primary OxPhos defects but also in a wide range of diseases, including neurodegenerative and immunological disorders. However, how central homeostatic and signalling pathways, such as mitophagy, fusion–fission, and mtDNA heteroplasmy levels, impact on the onset and progression of these diseases has only recently started to emerge. Thus, this is an exciting and thrilling new subject of investigation. Contributions to this Special Issue will provide a general overview and critical insight on our current understanding of these aspects. Our hope is to open a forum where the molecular mechanisms and pathophysiological consequences of mitochondrial dysfunction will be debated with the final aim of increassing our understanding of this emerging and exciting branch of mitochondrial biology and pathophysiology.

Dr. María Eugenia Soriano
Dr. Carlo Viscomi
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

  • mitochondria
  • mitochondrial dysfunction
  • mtDNA
  • heteroplasmy
  • fusion-fission unbalance
  • mitophagy
  • oxidative phosphorilation

Published Papers (1 paper)

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Review

Open AccessReview
Anti-Warburg Effect of Melatonin: A Proposed Mechanism to Explain its Inhibition of Multiple Diseases
Int. J. Mol. Sci. 2021, 22(2), 764; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020764 - 14 Jan 2021
Abstract
Glucose is an essential nutrient for every cell but its metabolic fate depends on cellular phenotype. Normally, the product of cytosolic glycolysis, pyruvate, is transported into mitochondria and irreversibly converted to acetyl coenzyme A by pyruvate dehydrogenase complex (PDC). In some pathological cells, [...] Read more.
Glucose is an essential nutrient for every cell but its metabolic fate depends on cellular phenotype. Normally, the product of cytosolic glycolysis, pyruvate, is transported into mitochondria and irreversibly converted to acetyl coenzyme A by pyruvate dehydrogenase complex (PDC). In some pathological cells, however, pyruvate transport into the mitochondria is blocked due to the inhibition of PDC by pyruvate dehydrogenase kinase. This altered metabolism is referred to as aerobic glycolysis (Warburg effect) and is common in solid tumors and in other pathological cells. Switching from mitochondrial oxidative phosphorylation to aerobic glycolysis provides diseased cells with advantages because of the rapid production of ATP and the activation of pentose phosphate pathway (PPP) which provides nucleotides required for elevated cellular metabolism. Molecules, called glycolytics, inhibit aerobic glycolysis and convert cells to a healthier phenotype. Glycolytics often function by inhibiting hypoxia-inducible factor-1α leading to PDC disinhibition allowing for intramitochondrial conversion of pyruvate into acetyl coenzyme A. Melatonin is a glycolytic which converts diseased cells to the healthier phenotype. Herein we propose that melatonin’s function as a glycolytic explains its actions in inhibiting a variety of diseases. Thus, the common denominator is melatonin’s action in switching the metabolic phenotype of cells. Full article
(This article belongs to the Special Issue Molecular Research on Mitochondrial Dysfunction)
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