Mitochondria at the Crossroad of Health and Disease—Second Edition

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 271

Special Issue Editor


E-Mail Website
Guest Editor
Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Interests: mitochondria; bioenergetics; neuron; calcium; neurodegeneration; cell death; Huntington's disease; Alzheimer's disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are the key organelles in the aerobic cell. They have multiple functions, which significantly impact cell life and death. Mitochondria are the main consumers of oxygen and producers of ATP, supporting energy-demanding processes in the cell. Mitochondrial oxidative metabolism unavoidably results in the generation of reactive oxygen species (ROS), which may significantly contribute to oxidative stress under pathological conditions. Mitochondria play a very important role in calcium signaling by taking up significant amounts of calcium during excessive calcium influx in the cell or substantial calcium release from endoplasmic reticulum. The calcium overload of mitochondria may induce a mitochondrial permeability transition pore that causes mitochondrial depolarization, leading to inhibition of ATP production in mitochondria, and mitochondrial swelling, resulting in the rupture of the mitochondrial outer membrane and release of cytochrome c and other apoptogenic proteins. Mitochondrial health is maintained by selective elimination of damaged organelles in the process of mitophagy. Mitochondrial dynamics, the ability to move along microtubules and undergo fragmentation (fission) and elongation (fusion), significantly contributes to mitochondrial quality control and elimination of damaged organelles. These processes are well-coordinated in healthy cells but can go awry in different pathologies, in aging, and in age-related diseases. There is a great deal of information about mitochondrial biology, but there are still a lot of unanswered questions regarding the functioning of healthy mitochondria and the mechanisms of mitochondrial dysfunction in aging and age-related pathologies. Consequently, this Special Issue is devoted to new developments in mitochondrial biology and is aimed at elucidating the mechanisms of mitochondrial dysfunction under various pathologies, in healthy aging and age-related diseases. We invite authors to contribute original research papers as well as review articles. We encourage authors to share their exciting recent findings addressing new developments in mitochondrial biology and clarifying the mechanisms of mitochondrial dysfunction under various conditions.

Prof. Dr. Nickolay Brustovetsky
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 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. Cells 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 2700 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
  • mitochondrial ion transport
  • permeability transition pore
  • mitochondrial ROS generation
  • mitochondrial quality control
  • mitochondrial traffic
  • mitochondrial morphology
  • mitochondrial dynamics
  • mitophagy

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue policies can be found here.

Related Special Issue

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

22 pages, 4136 KiB  
Article
Collapsin Response Mediator Protein 2 (CRMP2) Modulates Mitochondrial Oxidative Metabolism in Knock-In AD Mouse Model
by Tatiana Brustovetsky, Rajesh Khanna and Nickolay Brustovetsky
Cells 2025, 14(9), 647; https://doi.org/10.3390/cells14090647 (registering DOI) - 29 Apr 2025
Abstract
We explored how the phosphorylation state of collapsin response mediator protein 2 (CRMP2) influences mitochondrial functions in cultured cortical neurons and cortical synaptic mitochondria isolated from APP-SAA KI mice, a knock-in APP mouse model of Alzheimer’s disease (AD). CRMP2 phosphorylation was increased at [...] Read more.
We explored how the phosphorylation state of collapsin response mediator protein 2 (CRMP2) influences mitochondrial functions in cultured cortical neurons and cortical synaptic mitochondria isolated from APP-SAA KI mice, a knock-in APP mouse model of Alzheimer’s disease (AD). CRMP2 phosphorylation was increased at Thr 509/514 and Ser 522 in brain cortical lysates and cultured neurons from AD mice. The basal and maximal respiration of AD neurons were decreased. Mitochondria were hyperpolarized and superoxide anion production was increased in neurons from AD mice. In isolated synaptic AD mitochondria, ADP-stimulated and DNP-stimulated respiration were decreased, whereas ADP-induced mitochondrial depolarization was reduced and prolonged. We found that CRMP2 binds to the adenine nucleotide translocase (ANT) in a phosphorylation-dependent manner. The increased CRMP2 phosphorylation in AD mice correlated with CRMP2 dissociation from the ANT and decreased ANT activity in AD mitochondria. On the other hand, recombinant CRMP2 (rCRMP2), added to the ANT-reconstituted proteoliposomes, increased ANT activity. A small molecule (S)-lacosamide ((S)-LCM), which binds to CRMP2 and suppresses CRMP2 phosphorylation by Cdk5 and GSK-3β, prevented CRMP2 hyperphosphorylation, rescued CRMP2 binding to the ANT, improved ANT activity, and restored the mitochondrial membrane potential and respiratory responses to ADP and 2,4-dinitrophenol. Thus, our study highlights an important role for CRMP2 in regulating the mitochondrial oxidative metabolism in AD by modulating the ANT activity in a phosphorylation-dependent manner. Full article
(This article belongs to the Special Issue Mitochondria at the Crossroad of Health and Disease—Second Edition)
Show Figures

Figure 1

Back to TopTop