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Special Issue "Mitochondrial Bioenergetics in Different Pathophysiological Conditions"

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 March 2021.

Special Issue Editors

Dr. Anna Atlante
Website1 Website2
Guest Editor
Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies, National Council of Research, Bari, Italy
Interests: Mitochondrial bioenergetics; oxidative phosphorylation; mitochondrial dysfunction; metabolic regulation; oxidative stress; apoptosis; Alzheimer’s disease; cystic fibrosis
Dr. Daniela Valenti
Website
Guest Editor
Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies, National Council of Research, Bari, Italy
Interests: Mitochondrial bioenergetics; mitochondrial metabolism; mitochondrial transport; mitochondrial signaling pathways; mitochondrial dysfunction; neurodevelopmental diseases; oxidative stress; reactive oxygen species; programmed cell death

Special Issue Information

Dear Colleagues,

Mitochondria are central actors in the bioenergetics of cellular life. They are maternally inherited, multifunctional organelles widely known for generating energy in the form of ATP through the inner membrane mitochondrial respiratory chain complexes that form the functional respirasome. Besides the oxidative phosphorylation process, mitochondrial transport, inter-organelle crosstalk, mitochondrial dynamics, biogenesis and degradation all play a critical role in the efficiency and homeostasis of mitochondrial bioenergetics. Damage to these highly energetic and redox-sensitive organelles can result in an increase in the autophagic removal of the mitochondria (mitophagy) and disruption to the mitochondrial network. Mitochondrial dysfunction is now emerging as a major contributor to the pathogenesis of a broad range of human diseases, directly or indirectly, through a wide spectrum of signaling pathways.

Contributions to this Special Issue will provide new insights into mitochondrial bioenergetics to deepen our understanding of its role in health and disease and reveal novel mitochondria-targeting therapeutic opportunities. Original research articles and topical reviews on these and related topics are welcome in this Special Issue.

Dr. Anna Atlante
Dr. Daniela Valenti
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

  • mitochondrial ATP generation
  • oxidative phosphorylation machinery
  • mitochondrial quality control
  • mitochondrial dynamic network
  • mitogenesis/mitophagy
  • mitochondrial signaling
  • inter-organelle crosstalk
  • mitochondrial dysfunction
  • mitochondria-targeting therapeutic strategies

Published Papers (2 papers)

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Review

Open AccessReview
Mitochondrial Structure and Bioenergetics in Normal and Disease Conditions
Int. J. Mol. Sci. 2021, 22(2), 586; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020586 - 08 Jan 2021
Abstract
Mitochondria are ubiquitous intracellular organelles found in almost all eukaryotes and involved in various aspects of cellular life, with a primary role in energy production. The interest in this organelle has grown stronger with the discovery of their link to various pathologies, including [...] Read more.
Mitochondria are ubiquitous intracellular organelles found in almost all eukaryotes and involved in various aspects of cellular life, with a primary role in energy production. The interest in this organelle has grown stronger with the discovery of their link to various pathologies, including cancer, aging and neurodegenerative diseases. Indeed, dysfunctional mitochondria cannot provide the required energy to tissues with a high-energy demand, such as heart, brain and muscles, leading to a large spectrum of clinical phenotypes. Mitochondrial defects are at the origin of a group of clinically heterogeneous pathologies, called mitochondrial diseases, with an incidence of 1 in 5000 live births. Primary mitochondrial diseases are associated with genetic mutations both in nuclear and mitochondrial DNA (mtDNA), affecting genes involved in every aspect of the organelle function. As a consequence, it is difficult to find a common cause for mitochondrial diseases and, subsequently, to offer a precise clinical definition of the pathology. Moreover, the complexity of this condition makes it challenging to identify possible therapies or drug targets. Full article
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Open AccessReview
Mitochondrial Mechanisms of Necroptosis in Liver Diseases
Int. J. Mol. Sci. 2021, 22(1), 66; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22010066 - 23 Dec 2020
Abstract
Cell death represents a basic biological paradigm that governs outcomes and long-term sequelae in almost every hepatic disease. Necroptosis is a common form of programmed cell death in the liver. Necroptosis can be activated by ligands of death receptors, which then interact with [...] Read more.
Cell death represents a basic biological paradigm that governs outcomes and long-term sequelae in almost every hepatic disease. Necroptosis is a common form of programmed cell death in the liver. Necroptosis can be activated by ligands of death receptors, which then interact with receptor-interactive protein kinases 1 (RIPK1). RIPK1 mediates receptor interacting receptor-interactive protein kinases 3 (RIPK3) and mixed lineage kinase domain-like protein (MLKL) and necrosome formation. Regarding the molecular mechanisms of mitochondrial-mediated necroptosis, the RIPK1/RIPK3/MLKL necrosome complex can enhance oxidative respiration and generate reactive oxygen species, which can be a crucial factor in the susceptibility of cells to necroptosis. The necrosome complex is also linked to mitochondrial components such as phosphoglycerate mutase family member 5 (PGAM5), metabolic enzymes in the mitochondrial matrix, mitochondrial permeability protein, and cyclophilin D. In this review, we focus on the role of mitochondria-mediated cell necroptosis in acute liver injury, chronic liver diseases, and hepatocellular carcinoma, and its possible translation into clinical applications. Full article
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