Special Issue "Mitochondrial Function in Health and Disease"

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (31 May 2018).

Special Issue Editor

Dr. Kira Holmstrom
E-Mail Website
Guest Editor
University of Helsinki Institute of Biotechnology, Helsinki, Finland
University of Tampere BioMediTech, Tampere Finland
Interests: neurodegeneration; nervous system; mitochondria; alternative respiratory enzymes; mitochondrial calcium; reactive oxygen species

Special Issue Information

Dear Colleagues,

The mitochondrion is a complex organelle. In addition to being the main source of ATP production in most cells, it hosts and coordinates an array of functions from calcium sequestration and heme synthesis to cell death. Most mitochondrial functions rely on an intact respiratory chain and oxidative phosphorylation. One of the side effects of respiration is the production of reactive oxygen species (ROS) that can be damaging to the cell. At the same time, ROS has emerged as a potential signalling molecule in the cell. Growing awareness of mitochondrial involvement in an increasing number of diseases has led to a steady increase in medical mitochondrial research over the past decades.

This Special Issue aims to publish original research papers and reviews on aspects of mitochondrial function in various disorders ranging from aging and neurodegeneration to diabetes and cardiovascular disorders. It will focus on topics that relate to; how respiratory defects play a role in pathology; the functions of mitochondrial calcium; the influence of ROS on cell death; mitochondrial impact on redox homeostasis; the use of antioxidants for therapy; and agents that promote mitochondrial function as therapeutic targets.

Dr. Kira Holmstrom
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 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. 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 1400 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

  • Mitochondria
  • Oxidative phosphorylation
  • Oxidative stress
  • Cell death
  • Antioxidants
  • Calcium
  • Neurodegeneration
  • Aging
  • Diabetes
  • Cardiovascular disease

Published Papers (3 papers)

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Review

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Open AccessReview
A Disturbance in the Force: Cellular Stress Sensing by the Mitochondrial Network
Antioxidants 2018, 7(10), 126; https://doi.org/10.3390/antiox7100126 - 22 Sep 2018
Cited by 5
Abstract
As a highly dynamic organellar network, mitochondria are maintained as an organellar network by delicately balancing fission and fusion pathways. This homeostatic balance of organellar dynamics is increasingly revealed to play an integral role in sensing cellular stress stimuli. Mitochondrial fission/fusion balance is [...] Read more.
As a highly dynamic organellar network, mitochondria are maintained as an organellar network by delicately balancing fission and fusion pathways. This homeostatic balance of organellar dynamics is increasingly revealed to play an integral role in sensing cellular stress stimuli. Mitochondrial fission/fusion balance is highly sensitive to perturbations such as loss of bioenergetic function, oxidative stress, and other stimuli, with mechanistic contribution to subsequent cell-wide cascades including inflammation, autophagy, and apoptosis. The overlapping activity with m-AAA protease 1 (OMA1) metallopeptidase, a stress-sensitive modulator of mitochondrial fusion, and dynamin-related protein 1 (DRP1), a regulator of mitochondrial fission, are key factors that shape mitochondrial dynamics in response to various stimuli. As such, OMA1 and DRP1 are critical factors that mediate mitochondrial roles in cellular stress-response signaling. Here, we explore the current understanding and emerging questions in the role of mitochondrial dynamics in sensing cellular stress as a dynamic, responsive organellar network. Full article
(This article belongs to the Special Issue Mitochondrial Function in Health and Disease)
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Open AccessReview
Role of Presenilin in Mitochondrial Oxidative Stress and Neurodegeneration in Caenorhabditis elegans
Antioxidants 2018, 7(9), 111; https://doi.org/10.3390/antiox7090111 - 24 Aug 2018
Cited by 2
Abstract
Neurodegenerative diseases like Alzheimer’s disease (AD) are poised to become a global health crisis, and therefore understanding the mechanisms underlying the pathogenesis is critical for the development of therapeutic strategies. Mutations in genes encoding presenilin (PSEN) occur in most familial Alzheimer’s disease but [...] Read more.
Neurodegenerative diseases like Alzheimer’s disease (AD) are poised to become a global health crisis, and therefore understanding the mechanisms underlying the pathogenesis is critical for the development of therapeutic strategies. Mutations in genes encoding presenilin (PSEN) occur in most familial Alzheimer’s disease but the role of PSEN in AD is not fully understood. In this review, the potential modes of pathogenesis of AD are discussed, focusing on calcium homeostasis and mitochondrial function. Moreover, research using Caenorhabditis elegans to explore the effects of calcium dysregulation due to presenilin mutations on mitochondrial function, oxidative stress and neurodegeneration is explored. Full article
(This article belongs to the Special Issue Mitochondrial Function in Health and Disease)
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Other

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Open AccessPerspective
Chronic Inhibition of Mitochondrial Dihydrolipoamide Dehydrogenase (DLDH) as an Approach to Managing Diabetic Oxidative Stress
Antioxidants 2019, 8(2), 32; https://doi.org/10.3390/antiox8020032 - 02 Feb 2019
Abstract
Mitochondrial dihydrolipoamide dehydrogenase (DLDH) is a redox enzyme involved in decarboxylation of pyruvate to form acetyl-CoA during the cascade of glucose metabolism and mitochondrial adenine triphosphate (ATP) production. Depending on physiological or pathophysiological conditions, DLDH can either enhance or attenuate the production of [...] Read more.
Mitochondrial dihydrolipoamide dehydrogenase (DLDH) is a redox enzyme involved in decarboxylation of pyruvate to form acetyl-CoA during the cascade of glucose metabolism and mitochondrial adenine triphosphate (ATP) production. Depending on physiological or pathophysiological conditions, DLDH can either enhance or attenuate the production of reactive oxygen species (ROS) and reactive nitrogen species. Recent research in our laboratory has demonstrated that inhibition of DLDH induced antioxidative responses and could serve as a protective approach against oxidative stress in stroke injury. In this perspective article, we postulated that chronic inhibition of DLDH could also attenuate oxidative stress in type 2 diabetes. We discussed DLDH-involving mitochondrial metabolic pathways and metabolic intermediates that could accumulate upon DLDH inhibition and their corresponding roles in abrogating oxidative stress in diabetes. We also discussed a couple of DLDH inhibitors that could be tested in animal models of type 2 diabetes. It is our belief that DLDH inhibition could be a novel approach to fighting type 2 diabetes. Full article
(This article belongs to the Special Issue Mitochondrial Function in Health and Disease)
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