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Applied Sciences
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Mitochondria in Health and Disease
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Mitochondria in Health and Disease

A special issue of Applied Sciences (ISSN 2076-3417). This special issue belongs to the section "Applied Biosciences and Bioengineering".

Deadline for manuscript submissions: closed (10 November 2021) | Viewed by 7445

Special Issue Editors

Dr. Maria de la Encarnacion Solesio Torregrosa

E-Mail Website1 Website2
Guest Editor
Department of Biology, Rutgers-Camden, NJ 08102, USA
Interests: mitochondrial dysfunction; neurodegeneration; inorganic polyphosphate; polyP; aging; Alzheimer's disease; Parkinson's disease
Dr. Giuseppe Federico Amodeo

E-Mail Website
Guest Editor
Department of Neurology, Columbia University, New York, NY, USA
Interests: mitochondrial dysfunction; neurodegeneration; mitochondrial transport; misfolded proteins
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue of the journal Applied Sciences titled “Mitochondria in Health and Disease” aims to present recent advances on the mechanisms that regulate mitochondrial physiology and on those that drive mitochondrial dysfunction and failure in pathological conditions. Mitochondria play a key role in a wide variety of interconnected processes which are crucial for cellular survival, such as energey metabolism, calcium regulation, and apoptosis. Impairments of some of these processes have been broadly described in the etiopathology and in the consequences of many diseases.

Authors are invited to submit their latest results in mitochondrial research. Works conducted under physiological and/or pathological conditions are welcome. All papers need to present original, previously unpublished work and will be subjected to the standard peer-review processes of this journal. Potential topics of interest include but are not limited to: molecular structure of mitochondria and mitochondrial pores and channels, mechanisms of bioenergetics regulation and failure, characterization of mitochondrial dysfunction in various diseases, activation and regulation of apoptotic pathways and/or mitophagy.

We are looking forward to receiving your contributions.

Dr. Maria de la Encarnacion Solesio Torregrosa
Dr. Giuseppe Federico Amodeo
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. Applied Sciences is an international peer-reviewed open access semimonthly 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 2400 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 dysfunction
  • Mitochondrial physiology
  • Neurodegenerative disorders
  • Aging

Published Papers (2 papers)

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Research

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18 pages, 6699 KiB  
Article
Modeling the Effects of Calcium Overload on Mitochondrial Ultrastructural Remodeling
by Jasiel O. Strubbe-Rivera, Jiahui Chen, Benjamin A. West, Kristin N. Parent, Guo-Wei Wei and Jason N. Bazil
Appl. Sci. 2021, 11(5), 2071; https://doi.org/10.3390/app11052071 - 26 Feb 2021
Cited by 17 | Viewed by 3852
Abstract
Mitochondrial cristae are dynamic invaginations of the inner membrane and play a key role in its metabolic capacity to produce ATP. Structural alterations caused by either genetic abnormalities or detrimental environmental factors impede mitochondrial metabolic fluxes and lead to a decrease in their [...] Read more.
Mitochondrial cristae are dynamic invaginations of the inner membrane and play a key role in its metabolic capacity to produce ATP. Structural alterations caused by either genetic abnormalities or detrimental environmental factors impede mitochondrial metabolic fluxes and lead to a decrease in their ability to meet metabolic energy requirements. While some of the key proteins associated with mitochondrial cristae are known, very little is known about how the inner membrane dynamics are involved in energy metabolism. In this study, we present a computational strategy to understand how cristae are formed using a phase-based separation approach of both the inner membrane space and matrix space, which are explicitly modeled using the Cahn–Hilliard equation. We show that cristae are formed as a consequence of minimizing an energy function associated with phase interactions which are subject to geometric boundary constraints. We then extended the model to explore how the presence of calcium phosphate granules, entities that form in calcium overload conditions, exert a devastating inner membrane remodeling response that reduces the capacity for mitochondria to produce ATP. This modeling approach can be extended to include arbitrary geometrical constraints, the spatial heterogeneity of enzymes, and electrostatic effects to mechanize the impact of ultrastructural changes on energy metabolism. Full article
(This article belongs to the Special Issue Mitochondria in Health and Disease)
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Review

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17 pages, 882 KiB  
Review
The Relationship between Mitochondria and Neurodegeration in the Eye: A Review
by Hongtao Liu, Hanhan Liu and Verena Prokosch
Appl. Sci. 2021, 11(16), 7385; https://doi.org/10.3390/app11167385 - 11 Aug 2021
Cited by 5 | Viewed by 2851
Abstract
Mitochondria are the energy factories of cells. Mitochondrial dysfunction directly affects the function and morphology of cells. In recent years, growing evidence has shown that mitochondrial dysfunction plays an important role in neurodegenerative diseases. In the eye, some age-related diseases are considered to [...] Read more.
Mitochondria are the energy factories of cells. Mitochondrial dysfunction directly affects the function and morphology of cells. In recent years, growing evidence has shown that mitochondrial dysfunction plays an important role in neurodegenerative diseases. In the eye, some age-related diseases are considered to be neurodegenerative diseases, such as primary open-angle glaucoma (POAG) and age-related macular degeneration (AMD). Here, we review the mechanisms of mitochondrial damage, post-injury repair, and the roles of mitochondria in various tissues of the eye. In the following sections, the potential for treating glaucoma by reducing mitochondrial damage and promoting post-injury repair is also discussed. Full article
(This article belongs to the Special Issue Mitochondria in Health and Disease)
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