ijms-logo

Journal Browser

Journal Browser

Mitochondrial Function and Communication 2.0

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

Deadline for manuscript submissions: closed (30 August 2022) | Viewed by 4276

Special Issue Editor


E-Mail Website
Guest Editor
Department of Physiological Sciences, School of Medicine, University of Barcelona, Feixa Llarga s/n, 08907 L’Hospitalet del Llobregat, Spain
Interests: energy metabolism; metabolic plasticity; mitochondrial function; obesity related type 2 diabetes; exercise; lifestyle; integrative physiology; systems biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cellular functions that need an optimal interaction of mitochondria with other cellular components (endoplasmic reticulum, lipid droplets, lysosomes, nuclei) are relevant to energy metabolism, calcium handling, biosynthesis, anaplerosis and cataplerosis, proteostasis, autophagy, and apoptosis.

For correct functioning and meeting cellular needs, mitochondria adapt at different levels, from reorganization of the oxidative phosphorylation system, mitochondrial dynamics, and mitophagy to posttranslational modifications, differential gene expression, and biogenesis. All these processes are regulated by feedback mechanisms via exchange of information to other cellular compartments (metabolites, calcium, reactive oxygen species, and cytochrome c). Thus, recently, mitochondria have also been viewed as signaling organelles involved in intracellular communication and organ-crosstalk through mitokines that could signal via endocrine actions. Mitochondria can, therefore, alter metabolite signaling and nutrient handling, thus favoring other events triggered by intermediate lipid species (such as diacylglycerols and ceramides), hypoxia, epigenetics, or unbalanced amino acid profile.

For these reasons, mitochondrial dysfunction is directly implicated in the etiology of most chronic degenerative diseases and aging.

This Special Issue is dedicated to a series of studies that improve and update our current knowledge in mitochondrial function and communication both at the cellular level and systemically.

Dr. Pablo M. García-Rovés
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. 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 function
  • mitochondrial communication
  • mitochondrial proteostasis
  • anaplerosis
  • cataplerosis
  • mitophagy
  • apoptosis
  • mitochondria–lysosome crosstalk
  • mitochondrial dynamics
  • amino acid and lipid metabolism
  • mitokines

Related Special Issue

Published Papers (2 papers)

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

Research

14 pages, 2747 KiB  
Article
Rho/SRF Inhibitor Modulates Mitochondrial Functions
by Pankaj Patyal, Bachkhoa Nguyen, Xiaomin Zhang, Gohar Azhar, Fathima S. Ameer, Ambika Verma, Jasmine Crane, Grishma KC, Yingni Che and Jeanne Y. Wei
Int. J. Mol. Sci. 2022, 23(19), 11536; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911536 - 29 Sep 2022
Cited by 7 | Viewed by 1941
Abstract
CCG-1423 is a Rho A pathway inhibitor that has been reported to inhibit Rho/SRF-mediated transcriptional regulation. Serum response factor and its cofactors, which include ternary complex factors and myocardin-related transcription factors, regulate various cellular functions. In this study, we observed that CCG-1423 modulates [...] Read more.
CCG-1423 is a Rho A pathway inhibitor that has been reported to inhibit Rho/SRF-mediated transcriptional regulation. Serum response factor and its cofactors, which include ternary complex factors and myocardin-related transcription factors, regulate various cellular functions. In this study, we observed that CCG-1423 modulates the mitochondrial functions. The effect of this small molecule drug was determined by measuring mitochondrial function using an XFe96 Analyzer and an Oxygraph 2k (O2k) high-resolution respirometer. CCG-1423 treatment significantly reduced oxidative phosphorylation in a dose-dependent manner. However, CCG-1423 increased the glycolytic rate. We also observed that histone 4 at lysine-16 underwent hyperacetylation with the treatment of this drug. Immunolabeling with F-actin and MitoTracker revealed the alteration in the actin cytoskeleton and mitochondria. Taken together, our findings highlight a critical role of CCG-1423 in inhibiting the transcription of SRF/p49 and PGC-1α, β, resulting in the downregulation of mitochondrial genes, leading to the repression of mitochondrial oxidative phosphorylation and overall ATP reduction. This study provides a better understanding of the effects of CCG-1423 on mitochondria, which may be useful for the assessment of the potential clinical application of CCG-1423 and its derivatives. Full article
(This article belongs to the Special Issue Mitochondrial Function and Communication 2.0)
Show Figures

Figure 1

16 pages, 2246 KiB  
Article
Remodeling of Liver and Plasma Lipidomes in Mice Lacking Cyclophilin D
by Balazs Koszegi, Gabor Balogh, Zoltan Berente, Anett Vranesics, Edit Pollak, Laszlo Molnar, Aniko Takatsy, Viktoria Poor, Matyas Wahr, Csenge Antus, Krisztian Eros, Laszlo Vigh, Ferenc Gallyas, Jr., Maria Peter and Balazs Veres
Int. J. Mol. Sci. 2022, 23(19), 11274; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911274 - 24 Sep 2022
Viewed by 1651
Abstract
In recent years, several studies aimed to investigate the metabolic effects of non-functioning or absent cyclophilin D (CypD), a crucial regulatory component of mitochondrial permeability transition pores. It has been reported that the lack of CypD affects glucose and lipid metabolism. However, the [...] Read more.
In recent years, several studies aimed to investigate the metabolic effects of non-functioning or absent cyclophilin D (CypD), a crucial regulatory component of mitochondrial permeability transition pores. It has been reported that the lack of CypD affects glucose and lipid metabolism. However, the findings are controversial regarding the metabolic pathways involved, and most reports describe the effect of a high-fat diet on metabolism. We performed a lipidomic analysis of plasma and liver samples of CypD-/- and wild-type (WT) mice to reveal the lipid-specific alterations resulting from the absence of CypD. In the CypD-/- mice compared to the WT animals, we found a significant change in 52% and 47% of the measured 225 and 201 lipid species in liver and plasma samples, respectively. The higher total lipid content detected in these tissues was not accompanied by abdominal fat accumulation assessed by nuclear magnetic resonance imaging. We also documented characteristic changes in the lipid composition of the liver and plasma as a result of CypD ablation with the relative increase in polyunsaturated membrane lipid species. In addition, we did not observe remarkable differences in the lipid distribution of hepatocytes using histochemistry, but we found characteristic changes in the hepatocyte ultrastructure in CypD-/- animals using electron microscopy. Our results highlight the possible long-term effects of CypD inhibition as a novel therapeutic consideration for various diseases. Full article
(This article belongs to the Special Issue Mitochondrial Function and Communication 2.0)
Show Figures

Figure 1

Back to TopTop