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Mitochondria and Stress Responses
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Mitochondria and Stress Responses

A topical collection in Biology (ISSN 2079-7737). This collection belongs to the section "Cell Biology".

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Editor

Prof. Dr. Bernard Mignotte

E-Mail Website
Collection Editor
1. Laboratoire de Génétique et Biologie Cellulaire, UVSQ, Université Paris-Saclay, 78000 Versailles, France
2.Ecole Pratique des Hautes Etudes, PSL Research University, 75014 Paris, France
Interests: apoptosis; cell death; mitochondria; cell stress; mitophagy; aging; drosophila

Topical Collection Information

Dear Colleagues,

Mitochondria are generally known as the powerhouses of the cell. They play a central role in bioenergetics since they are the site of fatty acid β-oxidation, the tricarboxylic acid cycle, and oxidative phosphorylation. Mitochondria are also involved in various processes like pyrimidine synthesis, steroid hormone production, redox homeostasis, calcium storage, iron metabolism, etc. Mitochondria are involved in aging. They play a role in malignant tumor progression and respiratory chain dysfunctions, are responsible for multiple diseases referred to as mitochondriopathies, and defects in the mitochondrial network dynamics are associated with neurodegenerative disorders. According to this central position of mitochondria, various mechanisms involved in the quality control of the mitochondrial network have been selected during evolution. These mechanisms can operate at the protein level, using chaperones and proteases, at the organelle level (mitophagy), or at the cellular level (cell death). In addition to these responses to mitochondrial stress, mitochondria are also fully involved in the cell response to various stresses, such as DNA damage, viral infection, unbalanced proteostasis, and others. Notably, mitochondria are recognized today as central integrators of cell death and survival signals.

This Topical Collection entitled “Mitochondria and Stress Responses” aims to present articles focused on mitochondrial quality control mechanisms as well as on the role of mitochondria in cell stress responses. For example, articles dealing with subjects including but not restricted to mtUPR response, mitophagy, cell death processes involving mitochondria, and the crosstalk of mitochondria with other organelles are welcome, with an emphasis on recent developments in these fields. Original research and review articles are welcome.

Prof. Dr. Bernard Mignotte
Collection 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 collection 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. Biology 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 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
  • cell death
  • apoptosis
  • cell stress
  • mitophagy
  • aging
  • mitochondrial stress
  • mtUPR
  • mitochondrial quality control

Published Papers (6 papers)

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2024

Jump to: 2022, 2021, 2020

32 pages, 2160 KiB  
Review
ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor
by Adrien Corne, Florine Adolphe, Jérôme Estaquier, Sébastien Gaumer and Jean-Marc Corsi
Biology 2024, 13(3), 146; https://doi.org/10.3390/biology13030146 - 26 Feb 2024
Viewed by 1243
Abstract
Cellular integrated stress response (ISR), the mitochondrial unfolded protein response (UPRmt), and IFN signaling are associated with viral infections. Activating transcription factor 4 (ATF4) plays a pivotal role in these pathways and controls the expression of many genes involved in redox processes, amino [...] Read more.
Cellular integrated stress response (ISR), the mitochondrial unfolded protein response (UPRmt), and IFN signaling are associated with viral infections. Activating transcription factor 4 (ATF4) plays a pivotal role in these pathways and controls the expression of many genes involved in redox processes, amino acid metabolism, protein misfolding, autophagy, and apoptosis. The precise role of ATF4 during viral infection is unclear and depends on cell hosts, viral agents, and models. Furthermore, ATF4 signaling can be hijacked by pathogens to favor viral infection and replication. In this review, we summarize the ATF4-mediated signaling pathways in response to viral infections, focusing on human immunodeficiency virus 1 (HIV-1). We examine the consequences of ATF4 activation for HIV-1 replication and reactivation. The role of ATF4 in autophagy and apoptosis is explored as in the context of HIV-1 infection programmed cell deaths contribute to the depletion of CD4 T cells. Furthermore, ATF4 can also participate in the establishment of innate and adaptive immunity that is essential for the host to control viral infections. We finally discuss the putative role of the ATF4 paralogue, named ATF5, in HIV-1 infection. This review underlines the role of ATF4 at the crossroads of multiple processes reflecting host–pathogen interactions. Full article
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2022

Jump to: 2024, 2021, 2020

21 pages, 4951 KiB  
Article
A High-Throughput Search for SFXN1 Physical Partners Led to the Identification of ATAD3, HSD10 and TIM50
by Nesrine Tifoun, Mourad Bekhouche, José M. De las Heras, Arnaud Guillaume, Sylvina Bouleau, Isabelle Guénal, Bernard Mignotte and Nathalie Le Floch
Biology 2022, 11(9), 1298; https://doi.org/10.3390/biology11091298 - 31 Aug 2022
Cited by 3 | Viewed by 2287
Abstract
Sideroflexins (SFXN, SLC56) are a family of evolutionarily conserved mitochondrial carriers potentially involved in iron homeostasis. One member of the SFXN family is SFXN1, recently identified as a human mitochondrial serine transporter. However, little is known about the SFXN1 interactome, necessitating a high-throughput [...] Read more.
Sideroflexins (SFXN, SLC56) are a family of evolutionarily conserved mitochondrial carriers potentially involved in iron homeostasis. One member of the SFXN family is SFXN1, recently identified as a human mitochondrial serine transporter. However, little is known about the SFXN1 interactome, necessitating a high-throughput search to better characterize SFXN1 mitochondrial functions. Via co-immunoprecipitation followed by shotgun mass spectrometry (coIP-MS), we identified 96 putative SFXN1 interactors in the MCF7 human cell line. Our in silico analysis of the SFXN1 interactome highlights biological processes linked to mitochondrial organization, electron transport chains and transmembrane transport. Among the potential physical partners, ATAD3A and 17β-HSD10, two proteins associated with neurological disorders, were confirmed using different human cell lines. Nevertheless, further work will be needed to investigate the significance of these interactions. Full article
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2021

Jump to: 2024, 2022, 2020

13 pages, 2925 KiB  
Article
Effect of the MPT Pore Inhibitor Alisporivir on the Development of Mitochondrial Dysfunction in the Heart Tissue of Diabetic Mice
by Natalia V. Belosludtseva, Vlada S. Starinets, Irina B. Mikheeva, Dmitriy A. Serov, Maxim E. Astashev, Maxim N. Belosludtsev, Mikhail V. Dubinin and Konstantin N. Belosludtsev
Biology 2021, 10(9), 839; https://doi.org/10.3390/biology10090839 - 28 Aug 2021
Cited by 12 | Viewed by 2822
Abstract
Diabetes mellitus is a systemic metabolic disorder associated with mitochondrial dysfunction, with the mitochondrial permeability transition (MPT) pore opening being considered as one of its possible mechanisms. The effect of alisporivir, a non-immunosuppressive cyclosporin derivative and a selective inhibitor of the MPT pore [...] Read more.
Diabetes mellitus is a systemic metabolic disorder associated with mitochondrial dysfunction, with the mitochondrial permeability transition (MPT) pore opening being considered as one of its possible mechanisms. The effect of alisporivir, a non-immunosuppressive cyclosporin derivative and a selective inhibitor of the MPT pore opening, on the ultrastructure and functions of the heart mitochondria of mice with diabetes mellitus induced by a high-fat diet combined with streptozotocin injections was studied. The treatment of diabetic animals with alisporivir (2.5 mg/kg ip for 20 days) increased the rate of glucose clearance during the glucose tolerance test. The blood glucose level and the indicator of heart rate in alisporivir-treated diabetic mice tended to restore. An electron microscopy analysis showed that alisporivir prevented mitochondrial swelling and ultrastructural alterations in cardiomyocytes of diabetic mice. Alisporivir canceled the diabetes-induced increases in the susceptibility of heart mitochondria to the MPT pore opening and the level of lipid peroxidation products, but it did not affect the decline in mitochondrial oxidative phosphorylation capacity. The mRNA expression levels of Pink1 and Parkin in the heart tissue of alisporivir-treated diabetic mice were elevated, suggesting the stimulation of mitophagy. In parallel, alisporivir decreased the level of mtDNA in the heart tissue. These findings suggest that targeting the MPT pore opening by alisporivir alleviates the development of mitochondrial dysfunction in the diabetic heart. The cardioprotective effect of the drug in diabetes can be mediated by the induction of mitophagy and the inhibition of lipid peroxidation in the organelles. Full article
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14 pages, 3911 KiB  
Article
Unilateral Ureteral Obstruction for 28 Days in Rats Is Not Associated with Changes in Cardiac Function or Alterations in Mitochondrial Function
by Rodrigo Prieto-Carrasco, Alejandro Silva-Palacios, Pedro Rojas-Morales, Omar Emiliano Aparicio-Trejo, Estefany Ingrid Medina-Reyes, Estefani Yaquelin Hernández-Cruz, Carlos Sánchez-Garibay, Citlaltepetl Salinas-Lara, Natalia Pavón, Francisco Javier Roldán, Cecilia Zazueta, Edilia Tapia and José Pedraza-Chaverri
Biology 2021, 10(7), 671; https://doi.org/10.3390/biology10070671 - 16 Jul 2021
Cited by 6 | Viewed by 2497
Abstract
Our work evaluated cardiac function and mitochondrial bioenergetics parameters in hearts from male Wistar rats subjected to the UUO model during 28 days of progression. We measured markers of kidney damage and inflammation in plasma and renal fibrosis by histological analysis and Western [...] Read more.
Our work evaluated cardiac function and mitochondrial bioenergetics parameters in hearts from male Wistar rats subjected to the UUO model during 28 days of progression. We measured markers of kidney damage and inflammation in plasma and renal fibrosis by histological analysis and Western blot. Cardiac function was evaluated by echocardiography and proteins involved in cardiac damage by Western blot. Oxygen consumption and transmembrane potential were monitored in cardiac mitochondria using high-resolution respirometry. We also determined the activity of ATP synthase and antioxidant enzymes such as glutathione peroxidase, glutathione reductase, and catalase. Our results show that, although renal dysfunction is established in animals subjected to ureteral obstruction, cardiac function is maintained along with mitochondrial function and antioxidant enzymes activity after 28 days of injury evolution. Our results suggest that renocardiac syndrome might develop but belatedly in obstruction-induced renal damage, opening the opportunity for treatment to prevent this condition. Full article
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20 pages, 2572 KiB  
Review
The Impact of Mitochondrial Fission-Stimulated ROS Production on Pro-Apoptotic Chemotherapy
by Jan Ježek, Katrina F. Cooper and Randy Strich
Biology 2021, 10(1), 33; https://doi.org/10.3390/biology10010033 - 06 Jan 2021
Cited by 22 | Viewed by 3777
Abstract
Cancer is one of the world’s deadliest afflictions. Despite recent advances in diagnostic and surgical technologies, as well as improved treatments of some individual tumor types, there is currently no universal cure to prevent or impede the uncontrolled proliferation of malignant cells. Targeting [...] Read more.
Cancer is one of the world’s deadliest afflictions. Despite recent advances in diagnostic and surgical technologies, as well as improved treatments of some individual tumor types, there is currently no universal cure to prevent or impede the uncontrolled proliferation of malignant cells. Targeting tumors by inducing apoptosis is one of the pillars of cancer treatment. Changes in mitochondrial morphology precede intrinsic apoptosis, but mitochondrial dynamics has only recently been recognized as a viable pharmacological target. In many cancers, oncogenic transformation is accompanied by accumulation of elevated cellular levels of ROS leading to redox imbalance. Hence, a common chemotherapeutic strategy against such tumor types involves deploying pro-oxidant agents to increase ROS levels above an apoptotic death-inducing threshold. The aim of this chapter is to investigate the benefit of stimulating mitochondrial fission-dependent production of ROS for enhanced killing of solid tumors. The main question to be addressed is whether a sudden and abrupt change in mitochondrial shape toward the fragmented phenotype can be pharmacologically harnessed to trigger a burst of mitochondrial ROS sufficient to initiate apoptosis specifically in cancer cells but not in non-transformed healthy tissues. Full article
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2020

Jump to: 2024, 2022, 2021

18 pages, 1824 KiB  
Review
Mitochondrial microRNAs: A Putative Role in Tissue Regeneration
by Sílvia C. Rodrigues, Renato M. S. Cardoso and Filipe V. Duarte
Biology 2020, 9(12), 486; https://doi.org/10.3390/biology9120486 - 21 Dec 2020
Cited by 3 | Viewed by 3801
Abstract
The most famous role of mitochondria is to generate ATP through oxidative phosphorylation, a metabolic pathway that involves a chain of four protein complexes (the electron transport chain, ETC) that generates a proton-motive force that in turn drives the ATP synthesis by the [...] Read more.
The most famous role of mitochondria is to generate ATP through oxidative phosphorylation, a metabolic pathway that involves a chain of four protein complexes (the electron transport chain, ETC) that generates a proton-motive force that in turn drives the ATP synthesis by the Complex V (ATP synthase). An impressive number of more than 1000 mitochondrial proteins have been discovered. Since mitochondrial proteins have a dual genetic origin, it is predicted that ~99% of these proteins are nuclear-encoded and are synthesized in the cytoplasmatic compartment, being further imported through mitochondrial membrane transporters. The lasting 1% of mitochondrial proteins are encoded by the mitochondrial genome and synthesized by the mitochondrial ribosome (mitoribosome). As a result, an appropriate regulation of mitochondrial protein synthesis is absolutely required to achieve and maintain normal mitochondrial function. Regarding miRNAs in mitochondria, it is well-recognized nowadays that several cellular mechanisms involving mitochondria are regulated by many genetic players that originate from either nuclear- or mitochondrial-encoded small noncoding RNAs (sncRNAs). Growing evidence collected from whole genome and transcriptome sequencing highlight the role of distinct members of this class, from short interfering RNAs (siRNAs) to miRNAs and long noncoding RNAs (lncRNAs). Some of the mechanisms that have been shown to be modulated are the expression of mitochondrial proteins itself, as well as the more complex coordination of mitochondrial structure and dynamics with its function. We devote particular attention to the role of mitochondrial miRNAs and to their role in the modulation of several molecular processes that could ultimately contribute to tissue regeneration accomplishment. Full article
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