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Antioxidants
Special Issues
Oxidative Stress in Chronic and Age-Related Diseases
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Oxidative Stress in Chronic and Age-Related Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (15 December 2021) | Viewed by 19156

Special Issue Editor

Dr. Chiara Mozzini

E-Mail Website
Guest Editor
Department of Medicine, Section of Internal Medicine, University of Verona, 37134 Verona, Italy
Interests: cardiovascular diseases; atherosclerosis; inflammation; ultrasound; oxidative stress

Special Issue Information

Dear Colleagues,

The connection between oxidative stress and the main age-related diseases is an exciting field of research. Oxidative stress is involved in several age-related conditions (cardiovascular diseases, chronic obstructive pulmonary disease, chronic kidney disease, neurodegenerative diseases, and cancer, as well as sarcopenia and frailty). This Issue will discuss pre-clinical and clinical evidence highlighting the central role of oxidative stress in the progression of select chronic diseases. We will focus on atherosclerosis, chronic liver diseases, and chronic hematologic diseases, in particular on clonal haematopoiesis. In addition, ageing is also part of our Special Issue, because common mechanisms are shared by both chronic diseases and ageing. There will be particular focus on oxidative stress, as well as on inflammation and endoplasmic reticulum (ER) stress. The pathways regulated by nuclear factor E2 related factor (Nrf2) and nuclear factor kappa B (NF-kB), and related to the unfolded protein response (UPR) and ER stress are receiving increased attention as oxidative stress co-operators. I hope that this Issue will be a real eye-opener in the field of oxidative stress research in chronic and age-related diseases.

Dr. Chiara Mozzini
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

  • Oxidative stress
  • Atherosclerosis
  • Chronic liver diseases
  • Hematologic chronic disorders
  • Ageing

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Published Papers (6 papers)

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Editorial

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2 pages, 162 KiB  
Editorial
Oxidative Stress in Chronic and Age-Related Diseases
by Chiara Mozzini and Mauro Pagani
Antioxidants 2022, 11(3), 521; https://doi.org/10.3390/antiox11030521 - 8 Mar 2022
Cited by 10 | Viewed by 2433
Abstract
The connection between oxidative stress and common age-related diseases presents an exciting field of research [...] Full article
(This article belongs to the Special Issue Oxidative Stress in Chronic and Age-Related Diseases)

Research

Jump to: Editorial

14 pages, 3184 KiB  
Article
Potential Implications of Rimonabant on Age-Related Oxidative Stress and Inflammation
by Renáta Szabó, Zsuzsanna Szabó, Denise Börzsei, Alexandra Hoffmann, Zelma Nadin Lesi, Patrícia Pálszabó, Andrea Pálszabó, Szabolcs Dvorácskó, Rudolf Gesztelyi, Krisztina Kupai, Dániel Priksz, Béla Juhász, Anita Altmayer, Csaba Varga and Anikó Pósa
Antioxidants 2022, 11(1), 162; https://doi.org/10.3390/antiox11010162 - 14 Jan 2022
Cited by 6 | Viewed by 2834
Abstract
Over the last decades, growing interest has turned to preventive and therapeutic approaches for achieving successful aging. Oxidative stress and inflammation are fundamental features of cardiovascular diseases; therefore, potential targets of them can improve cardiac outcomes. Our study aimed to examine the involvement [...] Read more.
Over the last decades, growing interest has turned to preventive and therapeutic approaches for achieving successful aging. Oxidative stress and inflammation are fundamental features of cardiovascular diseases; therefore, potential targets of them can improve cardiac outcomes. Our study aimed to examine the involvement of the endocannabinoid system, especially the CB1 receptor blockade, on inflammatory and oxidant/antioxidant processes. Twenty-month-old female and male Wistar rats were divided into rimonabant-treated and aging control (untreated) groups. Rimonabant, a selective CB1 receptor antagonist, was administered at the dose of 1 mg/kg/day intraperitoneally for 2 weeks. Cardiac amounts of ROS, the antioxidant glutathione and superoxide dismutase (SOD), and the activity and concentration of the heme oxygenase (HO) enzyme were detected. Among inflammatory parameters, nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), and myeloperoxidase (MPO) enzyme activity were measured. Two weeks of low dose rimonabant treatment significantly reduced the cardiac ROS via boosting of the antioxidant defense mechanisms as regards the HO system, and the SOD and glutathione content. Consistently, the age-related inflammatory response was alleviated. Rimonabant-treated animals showed significantly decreased NF-κB, TNF-α, and MPO levels. Our findings prove the beneficial involvement of CB1 receptor blocker rimonabant on inflammatory and oxidative damages to the aging heart. Full article
(This article belongs to the Special Issue Oxidative Stress in Chronic and Age-Related Diseases)
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15 pages, 1954 KiB  
Article
Generation of Hydrogen Peroxide and Downstream Protein Kinase D1 Signaling Is a Common Feature of Inducers of Pancreatic Acinar-to-Ductal Metaplasia
by Heike R. Döppler, Geou-Yarh Liou and Peter Storz
Antioxidants 2022, 11(1), 137; https://doi.org/10.3390/antiox11010137 - 8 Jan 2022
Cited by 10 | Viewed by 2669
Abstract
Pancreatic acinar-to-ductal metaplasia (ADM) is a reversible process that occurs after pancreatic injury, but becomes permanent and leads to pancreatic lesions in the presence of an oncogenic mutation in KRAS,. While inflammatory macrophage-secreted chemokines, growth factors that activate epidermal growth factor receptor (EGFR) [...] Read more.
Pancreatic acinar-to-ductal metaplasia (ADM) is a reversible process that occurs after pancreatic injury, but becomes permanent and leads to pancreatic lesions in the presence of an oncogenic mutation in KRAS,. While inflammatory macrophage-secreted chemokines, growth factors that activate epidermal growth factor receptor (EGFR) and oncogenic KRAS have been implicated in the induction of ADM, it is currently unclear whether a common underlying signaling mechanism exists that drives this process. In this study, we show that different inducers of ADM increase levels of hydrogen peroxide, most likely generated at the mitochondria, and upregulate the expression of Protein Kinase D1 (PKD1), a kinase that can be activated by hydrogen peroxide. PKD1 expression in acinar cells affects their survival and mediates ADM, which is in part due to the PKD1 target NF-κB. Overall, our data implicate ROS-PKD1 signaling as a common feature of different inducers of pancreatic ADM. Full article
(This article belongs to the Special Issue Oxidative Stress in Chronic and Age-Related Diseases)
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19 pages, 2762 KiB  
Article
Jak2 Inhibitor AG490 Improved Poststroke Central and Peripheral Inflammation and Metabolic Abnormalities in a Rat Model of Ischemic Stroke
by Ya-Yu Wang, Shih-Yi Lin, Cheng-Yi Chang, Chih-Cheng Wu, Wen-Ying Chen, Su-Lan Liao, Yu-Fan Chen, Wen-Yi Wang and Chun-Jung Chen
Antioxidants 2021, 10(12), 1958; https://doi.org/10.3390/antiox10121958 - 7 Dec 2021
Cited by 8 | Viewed by 3242
Abstract
Poststroke hyperglycemia and inflammation have been implicated in the pathogenesis of stroke. Janus Kinase 2 (Jak2), a catalytic signaling component for cytokine receptors such as Interleukin-6 (IL-6), has inflammatory and metabolic properties. This study aimed to investigate the roles of Jak2 in poststroke [...] Read more.
Poststroke hyperglycemia and inflammation have been implicated in the pathogenesis of stroke. Janus Kinase 2 (Jak2), a catalytic signaling component for cytokine receptors such as Interleukin-6 (IL-6), has inflammatory and metabolic properties. This study aimed to investigate the roles of Jak2 in poststroke inflammation and metabolic abnormality in a rat model of permanent cerebral ischemia. Pretreatment with Jak2 inhibitor AG490 ameliorated neurological deficit, brain infarction, edema, oxidative stress, inflammation, caspase-3 activation, and Zonula Occludens-1 (ZO-1) reduction. Moreover, in injured cortical tissues, Tumor Necrosis Factor-α, IL-1β, and IL-6 levels were reduced with concurrent decreased NF-κB p65 phosphorylation, Signal Transducers and Activators of Transcription 3 phosphorylation, Ubiquitin Protein Ligase E3 Component N-Recognin 1 expression, and Matrix Metalloproteinase activity. In the in vitro study on bEnd.3 endothelial cells, AG490 diminished IL-6-induced endothelial barrier disruption by decreasing ZO-1 decline. Metabolically, administration of AG490 lowered fasting glucose, with improvements in glucose intolerance, plasma-free fatty acids, and plasma C Reactive Proteins. In conclusion, AG490 improved the inflammation and oxidative stress of neuronal, hepatic, and muscle tissues of stroke rats as well as impairing insulin signaling in the liver and skeletal muscles. Therefore, Jak2 blockades may have benefits for combating poststroke central and peripheral inflammation, and metabolic abnormalities. Full article
(This article belongs to the Special Issue Oxidative Stress in Chronic and Age-Related Diseases)
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14 pages, 2457 KiB  
Article
Effects of Folinic Acid Administration on Lower Limb Ischemia/Reperfusion Injury in Rats
by Iñigo Cearra, Borja Herrero de la Parte, Inmaculada Ruiz Montesinos, Ana Alonso-Varona, Diana Isabel Moreno-Franco and Ignacio García-Alonso
Antioxidants 2021, 10(12), 1887; https://doi.org/10.3390/antiox10121887 - 25 Nov 2021
Cited by 10 | Viewed by 2705
Abstract
Surgery under ischemic conditions, lasting up to 3 h, is routinely performed in orthopedic surgery, causing undesirable injury due to ischemia-reperfusion syndrome, with short and medium-term functional repercussions. To date, there is no established prophylactic treatment. In this work we evaluated folinic acid [...] Read more.
Surgery under ischemic conditions, lasting up to 3 h, is routinely performed in orthopedic surgery, causing undesirable injury due to ischemia-reperfusion syndrome, with short and medium-term functional repercussions. To date, there is no established prophylactic treatment. In this work we evaluated folinic acid (FA) in a rodent model of lower limb ischemia-reperfusion (IRI-LL). 36 male WAG rats underwent 3 h of lower limb ischemia. In the saline group, rats received intraperitoneal administration of saline (used as vehicle for treatment). In the experimental group, rats were pretreated with FA (2.5 mg/kg) before the end of ischemia. After ischemia, animals were sacrificed at 3 h, 24 h or 14 days (for biochemical determination (Na+, K+, Cl-, urea, creatinine, CK, LDH, ALP, ALT, and AST), pathological assessment, or functional study using the rotarod test; respectively). Another six animals were used to establish the reference values. The prophylactic administration of FA significantly reduced the elevation of biochemical markers, especially those that most directly indicate muscle damage (CK and LDH). In addition, it also improved direct tissue damage, both in terms of edema, weight, PMN infiltrate and percentage of damaged fibers. Finally, the administration of FA allowed the animals to equal baseline values in the rotarod test; what did not occur in the saline group, where pre-ischemia levels were not recovered. Following 3 h of lower limb ischemia, FA minimizes the increase of CK and LDH, as well as local edema and leukocyte infiltration, allowing a faster recovery of limb functionality. Therefore, it could be considered as a prophylactic treatment when tourniquet is used in clinics. Full article
(This article belongs to the Special Issue Oxidative Stress in Chronic and Age-Related Diseases)
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22 pages, 3053 KiB  
Article
Cimicifuga racemosa Extract Ze 450 Re-Balances Energy Metabolism and Promotes Longevity
by Malena Rabenau, Benjamin Dillberger, Madeline Günther, Sylvia Krippner, Veronika Butterweck, Georg Boonen, Jürgen Drewe, Gunter P. Eckert and Carsten Culmsee
Antioxidants 2021, 10(9), 1432; https://doi.org/10.3390/antiox10091432 - 8 Sep 2021
Cited by 9 | Viewed by 4211
Abstract
Recently, we reported that the Cimicifuga racemosa extract Ze 450 mediated protection from oxidative cell damage through a metabolic shift from oxidative phosphorylation to glycolysis. Here, we investigated the molecular mechanisms underlying the effects of Ze 450 against ferroptosis in neuronal cells, with [...] Read more.
Recently, we reported that the Cimicifuga racemosa extract Ze 450 mediated protection from oxidative cell damage through a metabolic shift from oxidative phosphorylation to glycolysis. Here, we investigated the molecular mechanisms underlying the effects of Ze 450 against ferroptosis in neuronal cells, with a particular focus on mitochondria. The effects of Ze 450 on respiratory complex activity and hallmarks of ferroptosis were studied in isolated mitochondria and in cultured neuronal cells, respectively. In addition, Caenorhabditis elegans served as a model organism to study mitochondrial damage and longevity in vivo. We found that Ze 450 directly inhibited complex I activity in mitochondria and enhanced the metabolic shift towards glycolysis via cMyc and HIF1α regulation. The protective effects against ferroptosis were mediated independently of estrogen receptor activation and were distinct from effects exerted by metformin. In vivo, Ze 450 protected C. elegans from the mitochondrial toxin paraquat and promoted longevity in a dose-dependent manner. In conclusion, Ze 450 mediated a metabolic shift to glycolysis via direct effects on mitochondria and altered cell signaling, thereby promoting sustained cellular resilience to oxidative stress in vitro and in vivo. Full article
(This article belongs to the Special Issue Oxidative Stress in Chronic and Age-Related Diseases)
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