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Antioxidants
Special Issues
Mitochondrial Reactive Species in Physiology and Pathology
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Mitochondrial Reactive Species in Physiology and Pathology

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "ROS, RNS and RSS".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 6179

Special Issue Editor

Dr. Laurent Chatre

E-Mail Website
Guest Editor
ISTCT, CERVOxy team, UMR 6030-CNRS, Université de Caen-Normandie, CEA, GIP Cyceron, Caen, France
Interests: mitochondria; reactive species; stress; bioenergetic metabolism; protease; cancer; aging; inflammation; brain; neurodegenerative disease

Special Issue Information

Dear Colleagues, 

From the first definition of “stress” in 1925 by Hans Selye, the “oxidative stress” definition from the redox pioneer Helmut Sies in 1985, and the “oxidative eustress and distress” definition in 2017 by Helmut Sies, to the most recent definition, Reactive Species Interactome (RSI), in 2017 by Cortese-Krott et al., there are still many unanswered questions and perspectives concerning physiology and pathology, including in the respiratory organelle, mitochondria. 

A deeper understanding of oxidative eustress and distress is important through the reactive oxygen species (ROS), the reactive nitrogen species (RNS), the reactive sulfur species (RSS), and the reactive carbonyl species (RCS). This Special issue focuses on the roles of these reactive species in relation to their concentration in mitochondrial physiology and disorders. 

Authors are invited to submit their latest findings or review articles to this Special Issue, which will bring together current research concerning the roles of the mitochondrial reactive species in bioenergetic metabolism, cell death, calcium homeostasis, and a variety of other mechanisms. The article must include at least two different reactive species families, and can include both in vitro and in vivo studies. 

I look forward to your contribution. 

Dr. Laurent Chatre
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. 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 2900 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
  • reactive species
  • ROS
  • RNS
  • RSS
  • RCS
  • energy
  • cell death
  • physiology
  • pathology

Published Papers (2 papers)

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Research

24 pages, 4111 KiB  
Article
Altered Mitochondrial Opa1-Related Fusion in Mouse Promotes Endothelial Cell Dysfunction and Atherosclerosis
by Ahmad Chehaitly, Anne-Laure Guihot, Coralyne Proux, Linda Grimaud, Jade Aurrière, Benoit Legouriellec, Jordan Rivron, Emilie Vessieres, Clément Tétaud, Antonio Zorzano, Vincent Procaccio, Françoise Joubaud, Pascal Reynier, Guy Lenaers, Laurent Loufrani and Daniel Henrion
Antioxidants 2022, 11(6), 1078; https://doi.org/10.3390/antiox11061078 - 28 May 2022
Cited by 12 | Viewed by 2685
Abstract
Flow (shear stress)-mediated dilation (FMD) of resistance arteries is a rapid endothelial response involved in tissue perfusion. FMD is reduced early in cardiovascular diseases, generating a major risk factor for atherosclerosis. As alteration of mitochondrial fusion reduces endothelial cells’ (ECs) sprouting and angiogenesis, [...] Read more.
Flow (shear stress)-mediated dilation (FMD) of resistance arteries is a rapid endothelial response involved in tissue perfusion. FMD is reduced early in cardiovascular diseases, generating a major risk factor for atherosclerosis. As alteration of mitochondrial fusion reduces endothelial cells’ (ECs) sprouting and angiogenesis, we investigated its role in ECs responses to flow. Opa1 silencing reduced ECs (HUVECs) migration and flow-mediated elongation. In isolated perfused resistance arteries, FMD was reduced in Opa1+/− mice, a model of the human disease due to Opa1 haplo-insufficiency, and in mice with an EC specific Opa1 knock-out (EC-Opa1). Reducing mitochondrial oxidative stress restored FMD in EC-Opa1 mice. In isolated perfused kidneys from EC-Opa1 mice, flow induced a greater pressure, less ATP, and more H2O2 production, compared to control mice. Opa1 expression and mitochondrial length were reduced in ECs submitted in vitro to disturbed flow and in vivo in the atheroprone zone of the mouse aortic cross. Aortic lipid deposition was greater in Ldlr−/--Opa1+/- and in Ldlr−/--EC-Opa1 mice than in control mice fed with a high-fat diet. In conclusion, we found that reduction in mitochondrial fusion in mouse ECs altered the dilator response to shear stress due to excessive superoxide production and induced greater atherosclerosis development. Full article
(This article belongs to the Special Issue Mitochondrial Reactive Species in Physiology and Pathology)
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14 pages, 1305 KiB  
Article
Plasma Free Thiol Levels during Early Sepsis Predict Future Renal Function Decline
by Elisabeth C. van der Slikke, Lisanne Boekhoud, Arno R. Bourgonje, Tycho J. Olgers, Jan C. ter Maaten, Robert H. Henning, Harry van Goor and Hjalmar R. Bouma
Antioxidants 2022, 11(5), 800; https://doi.org/10.3390/antiox11050800 - 19 Apr 2022
Cited by 4 | Viewed by 2342
Abstract
Sepsis is a life-threatening syndrome characterized by acute organ dysfunction due to infection. In particular, acute kidney injury (AKI) is common among patients with sepsis and is associated with increased mortality and morbidity. Oxidative stress is an important contributor to the pathogenesis of [...] Read more.
Sepsis is a life-threatening syndrome characterized by acute organ dysfunction due to infection. In particular, acute kidney injury (AKI) is common among patients with sepsis and is associated with increased mortality and morbidity. Oxidative stress is an important contributor to the pathogenesis of sepsis-related AKI. Plasma free thiols (R-SH) reflect systemic oxidative stress since they are readily oxidized by reactive species and thereby serve as antioxidants. Here, we aimed to assess the concentrations of serum free thiols in sepsis and associate these with major adverse kidney events (MAKE). Adult non-trauma patients who presented at the emergency department (ED) with a suspected infection were included. Free thiol levels and ischemia-modified albumin (IMA), a marker of oxidative stress, were measured in plasma at baseline, at the ward, and at three months, and one year after hospitalization. Plasma free thiol levels were lower at the ED visit and at the ward as compared to three months and one year after hospital admission (p < 0.01). On the contrary, plasma levels of IMA were higher at the ED and at the ward compared to three months and one year after hospital admission (p < 0.01). Furthermore, univariate logistic regression analyses showed that plasma free thiol levels at the ED were inversely associated with long-term renal function decline and survival at 90 days (MAKE90) and 365 days (MAKE365) (OR 0.43 per standard deviation [SD] [0.22–0.82, 95% CI], p = 0.011 and OR 0.58 per SD [0.34–0.96, 95% CI], p = 0.035, respectively). A multivariate regression analysis revealed an independent association of plasma free thiols at the ED (OR 0.52 per SD [0.29–0.93, 95% CI], p = 0.028) with MAKE365, even after adjustments for age, eGFR at the ED, SOFA score, and cardiovascular disease. These data indicate the clear role of oxidative stress in the pathogenesis of sepsis-AKI, as reflected in the lower plasma free thiol levels and increased levels of IMA. Full article
(This article belongs to the Special Issue Mitochondrial Reactive Species in Physiology and Pathology)
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