Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Mitochondria in Cell Death: Novel Partners and Perspectives
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Mitochondria in Cell Death: Novel Partners and Perspectives

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

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 13135

Special Issue Editors

Prof. Dr. Manuela Côrte-Real

E-Mail Website
Guest Editor
Centre of Molecular and Environmental Biology (CBMA), Department of Biology, University of Minho, 4710-057 Braga, Portugal
Interests: regulated cell death; mitochondrial dysfunctions; cancer/yeast cells; anticancer/antifungal activities; lactoferrin
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Maria João Sousa

E-Mail Website
Guest Editor
Centro de Biologia Molecular e Ambiental, Departamento de Biologia, Universidade do Minho, Braga, Portugal
Interests: regulated cell death; mitochondria; ER–mitochondria contact sites; vacuole/lysosomal permeabilization; yeast; metabolism; genome-wide analysis; new compounds; cytotoxicity
Dr. Susana R. Chaves

E-Mail Website
Guest Editor
Centro de Biologia Molecular e Ambiental, Departamento de Biologia, Universidade do Minho, Braga, Portugal
Interests: cell death; mitochondrial function; microbiology; molecular targets; cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Regulated cell death is a complex process involving a cascade of events that leads to elimination of a damaged, infected or useless cell committed to die. When unproperly executed, it compromises both development and homeostasis of multicellular organisms. Dysfunctions of cell death processes are therefore associated with different human diseases. Though extensive studies on different mechanisms underlying cell death have been carried out so far, a deeper understanding of the available cell processes and their regulation still continues to deserve particular attention due to its impact on the treatment of different human pathologies.

Mitochondria were identified early on as key organelles in the coordinated cell dismantling process, through the release of pro-death factors from the mitochondrial intermembrane space. More recently, its crosstalk with other organelles began to be addressed, adding more complexity to the involvement of mitochondria in cell death. Nonetheless, further studies are needed to identify new potential players and clarify mitochondrial-mediated pathways, including those involving other organelles. These could be pharmacologically targeted and thus exploited in the design of therapeutic strategies to counteract cell death deregulation associated with human disorders, such as cancer and neurodegeneration.

This Special Issue aims to provide an overview of current advances in the field of cell death with particular focus on the central role of mitochondria and its interaction with other organelles, aiming to better understand the multiple components and the complex interaction network involved. Contributions from both mammalian and non-mammalian eukaryotic cell models are welcome.

Prof. Dr. Manuela Côrte-Real
Prof. Dr. Maria João Sousa
Dr. Susana Chaves
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. 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

  • regulated cell death
  • mitochondrial outer membrane permeabilization
  • mitochondrial pro-death factors
  • vacuole
  • lysosome
  • endoplasmic reticulum-mitochondrial contacts
  • organelle crosstalk yeast
  • mammalian cell lines
  • cancer
  • neurodegenarative diseases

Published Papers (5 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

15 pages, 1835 KiB  
Article
Carbenoxolon Is Capable to Regulate the Mitochondrial Permeability Transition Pore Opening in Chronic Alcohol Intoxication
by Yulia Baburina, Irina Odinokova and Olga Krestinina
Int. J. Mol. Sci. 2021, 22(19), 10249; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910249 - 23 Sep 2021
Cited by 2 | Viewed by 1629
Abstract
Background: carbenoxolone, which is a derivative of glyceretic acid, is actively used in pharmacology for the treatment of diseases of various etiologies. In addition, we have shown carbenoxolone as an effective inducer of mitochondrial permeability transition pore in rat brain and liver mitochondria. [...] Read more.
Background: carbenoxolone, which is a derivative of glyceretic acid, is actively used in pharmacology for the treatment of diseases of various etiologies. In addition, we have shown carbenoxolone as an effective inducer of mitochondrial permeability transition pore in rat brain and liver mitochondria. Methods: in the course of this work, comparative studies were carried out on the effect of carbenoxolone on the parameters of mPTP functioning in mitochondria isolated from the liver of control and alcoholic rats. Results: within the framework of this work, it was found that carbenoxolone significantly increased its effect in the liver mitochondria of rats with chronic intoxication. In particular, this was expressed in a reduction in the lag phase, a decrease in the threshold calcium concentration required to open a pore, an acceleration of high-amplitude cyclosporin-sensitive swelling of mitochondria, as well as an increase in the effect of carbenoxolone on the level of mitochondrial membrane-bound proteins. Thus, as a result of the studies carried out, it was shown that carbenoxolone is involved in the development/modulation of alcohol tolerance and dependence in rats. Full article
(This article belongs to the Special Issue Mitochondria in Cell Death: Novel Partners and Perspectives)
►▼ Show Figures

Figure 1

17 pages, 3178 KiB  
Article
Neuroprotective Effect of a Novel ATP-Synthase Inhibitor Bedaquiline in Cerebral Ischemia-Reperfusion Injury
by Danielius Umbrasas, Odeta Arandarcikaite, Ramune Grigaleviciute, Rimantas Stakauskas and Vilmante Borutaite
Int. J. Mol. Sci. 2021, 22(18), 9717; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22189717 - 08 Sep 2021
Cited by 1 | Viewed by 2203
Abstract
Mitochondrial dysfunction during ischemic stroke ultimately manifests as ATP depletion. Mitochondrial ATP synthase upon loss of mitochondrial membrane potential during ischemia rapidly hydrolyses ATP and thus contributes to ATP depletion. Increasing evidence suggests that inhibition of ATP synthase limits ATP depletion and is [...] Read more.
Mitochondrial dysfunction during ischemic stroke ultimately manifests as ATP depletion. Mitochondrial ATP synthase upon loss of mitochondrial membrane potential during ischemia rapidly hydrolyses ATP and thus contributes to ATP depletion. Increasing evidence suggests that inhibition of ATP synthase limits ATP depletion and is protective against ischemic tissue damage. Bedaquiline (BDQ) is an anti-microbial agent, approved for clinical use, that inhibits ATP synthase of Mycobacteria; however recently it has been shown to act on mitochondrial ATP synthase, inhibiting both ATP synthesis and hydrolysis in low micromolar concentrations. In this study, we investigated whether preconditioning with BDQ can alleviate ischemia/reperfusion-induced brain injury in Wistar rats after middle cerebral artery occlusion-reperfusion and whether it affects mitochondrial functions. We found that BDQ was effective in limiting necrosis and neurological dysfunction during ischemia-reperfusion. BDQ also caused inhibition of ATPase activity, mild uncoupling of respiration, and stimulated mitochondrial respiration both in healthy and ischemic mitochondria. Mitochondrial calcium retention capacity was unaffected by BDQ preconditioning. We concluded that BDQ has neuroprotective properties associated with its action on mitochondrial respiration and ATPase activity. Full article
(This article belongs to the Special Issue Mitochondria in Cell Death: Novel Partners and Perspectives)
►▼ Show Figures

Figure 1

18 pages, 25301 KiB  
Article
Targeting Mitochondrial Metabolism in Clear Cell Carcinoma of the Ovaries
by Xiaonan Zhang, Mihir Shetty, Valentino Clemente, Stig Linder and Martina Bazzaro
Int. J. Mol. Sci. 2021, 22(9), 4750; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094750 - 29 Apr 2021
Cited by 6 | Viewed by 2862
Abstract
Ovarian clear cell carcinoma (OCCC) is a rare but chemorefractory tumor. About 50% of all OCCC patients have inactivating mutations of ARID1A, a member of the SWI/SNF chromatin-remodeling complex. Members of the SWI/SNF remodeling have emerged as regulators of the energetic metabolism [...] Read more.
Ovarian clear cell carcinoma (OCCC) is a rare but chemorefractory tumor. About 50% of all OCCC patients have inactivating mutations of ARID1A, a member of the SWI/SNF chromatin-remodeling complex. Members of the SWI/SNF remodeling have emerged as regulators of the energetic metabolism of mammalian cells; however, the role of ARID1A as a modulator of the mitochondrial metabolism in OCCCs is yet to be defined. Here, we show that ARID1A loss results in increased mitochondrial metabolism and renders ARID1A-mutated cells increasingly and selectively dependent on it. The increase in mitochondrial activity following ARID1A loss is associated with increase in c-Myc expression and increased mitochondrial number and reduction of their size consistent with a higher mitochondrial cristae/outer membrane ratio. Significantly, preclinical testing of the complex I mitochondrial inhibitor IACS-010759 showed it extends overall survival in a preclinical model of ARID1A-mutated OCCC. These findings provide for the targeting mitochondrial activity in ARID1A-mutated OCCCs. Full article
(This article belongs to the Special Issue Mitochondria in Cell Death: Novel Partners and Perspectives)
►▼ Show Figures

Figure 1

16 pages, 5476 KiB  
Article
Protective Effect of Quercetin on Sodium Iodate-Induced Retinal Apoptosis through the Reactive Oxygen Species-Mediated Mitochondrion-Dependent Pathway
by Yuan-Yen Chang, Yi-Ju Lee, Min-Yen Hsu, Meilin Wang, Shang-Chun Tsou, Ching-Chung Chen, Jer-An Lin, Yai-Ping Hsiao and Hui-Wen Lin
Int. J. Mol. Sci. 2021, 22(8), 4056; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22084056 - 14 Apr 2021
Cited by 16 | Viewed by 3644
Abstract
Age-related macular degeneration (AMD) leads to gradual central vision loss and is the third leading cause of irreversible blindness worldwide. The underlying mechanisms for this progressive neurodegenerative disease remain unclear and there is currently no preventive treatment for dry AMD. Sodium iodate (NaIO [...] Read more.
Age-related macular degeneration (AMD) leads to gradual central vision loss and is the third leading cause of irreversible blindness worldwide. The underlying mechanisms for this progressive neurodegenerative disease remain unclear and there is currently no preventive treatment for dry AMD. Sodium iodate (NaIO3) has been reported to induce AMD-like retinal pathology in mice. We established a mouse model for AMD to evaluate the effects of quercetin on NaIO3-induced retinal apoptosis, and to investigate the pertinent underlying mechanisms. Our in vitro results indicated that quercetin protected human retinal pigment epithelium (ARPE-19) cells from NaIO3-induced apoptosis by inhibiting reactive oxygen species production and loss of mitochondrial membrane potential as detected by Annexin V-FITC/PI flow cytometry. We also evaluated the relative expression of proteins in the apoptosis pathway. Quercetin downregulated the protein expressions of Bax, cleaved caspase-3, and cleaved PARP and upregulated the expression of Bcl-2 through reduced PI3K and pAKT expressions. Furthermore, our in vivo results indicated that quercetin improved retinal deformation and increased the thickness of both the outer nuclear layer and inner nuclear layer, whereas the expression of caspase-3 was inhibited. Taken together, these results demonstrate that quercetin could protect retinal pigment epithelium and the retina from NaIO3-induced cell apoptosis via reactive oxygen species-mediated mitochondrial dysfunction, involving the PI3K/AKT signaling pathway. This suggests that quercetin has the potential to prevent and delay AMD and other retinal diseases involving NaIO3-mediated apoptosis. Full article
(This article belongs to the Special Issue Mitochondria in Cell Death: Novel Partners and Perspectives)
►▼ Show Figures

Figure 1

18 pages, 4805 KiB  
Article
LONP1 Regulates Mitochondrial Accumulations of HMGB1 and Caspase-3 in CA1 and PV Neurons Following Status Epilepticus
by Ji-Eun Kim, Hana Park, Tae-Hyun Kim and Tae-Cheon Kang
Int. J. Mol. Sci. 2021, 22(5), 2275; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052275 - 25 Feb 2021
Cited by 10 | Viewed by 2095
Abstract
Lon protease 1 (LONP1) is a highly conserved serine peptidase that plays an important role in the protein quality control system in mammalian mitochondria. LONP1 catalyzes the degradation of oxidized, dysfunctional, and misfolded matrix proteins inside mitochondria and regulates mitochondrial gene expression and [...] Read more.
Lon protease 1 (LONP1) is a highly conserved serine peptidase that plays an important role in the protein quality control system in mammalian mitochondria. LONP1 catalyzes the degradation of oxidized, dysfunctional, and misfolded matrix proteins inside mitochondria and regulates mitochondrial gene expression and genome integrity. Therefore, LONP1 is up-regulated and suppresses cell death in response to oxidative stress, heat shock, and nutrient starvation. On the other hand, translocation of high mobility group box 1 (HMGB1) and active caspase-3 into mitochondria is involved in apoptosis of parvalbumin (PV) cells (one of the GABAergic interneurons) and necrosis of CA1 neurons in the rat hippocampus, respectively, following status epilepticus (SE). In the present study, we investigated whether LONP1 may improve neuronal viability to prevent or ameliorate translocation of active caspase-3 and HMGB1 in mitochondria within PV and CA1 neurons. Following SE, LONP1 expression was up-regulated in mitochondria of PV and CA1 neurons. LONP1 knockdown deteriorated SE-induced neuronal death with mitochondrial accumulation of active caspase-3 and HMGB1 in PV cells and CA1 neurons, respectively. LONP1 knockdown did not affect the aberrant mitochondrial machinery induced by SE. Therefore, our findings suggest, for the first time, that LONP1 may contribute to the alleviation of mitochondrial overloads of active caspase-3 and HMGB1, and the maintenance of neuronal viability against SE. Full article
(This article belongs to the Special Issue Mitochondria in Cell Death: Novel Partners and Perspectives)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop