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Antioxidants
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The Role of the Renin–Angiotensin System in Oxidative-Stress-Related Mechanisms in...
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The Role of the Renin–Angiotensin System in Oxidative-Stress-Related Mechanisms in Neurodegenerative 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 (31 March 2024) | Viewed by 7388

Special Issue Editors

Prof. Dr. Jose L. Labandeira-Garcia

E-Mail Website
Guest Editor
1. Research Center for Molecular Medicine and Chronic Diseases (CIMUS), IDIS, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain
2. Networking Research Center on Neurodegenerative Diseases (CIBERNED), 28031 Madrid, Spain
Interests: neurodegeneration; Parkinson’s disease; renin-angiotensin system
Dr. Ana I. Rodríguez-Pérez

E-Mail Website
Guest Editor
1. Research Center for Molecular Medicine and Chronic Diseases (CIMUS), IDIS, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain
2. Networking Research Center on Neurodegenerative Diseases (CIBERNED), 28031 Madrid, Spain
Interests: neurodegeneration; Parkinson’s disease; renin-angiotensin system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The renin–angiotensin system (RAS) was initially considered a circulating hormonal system that played a major role in the regulation of blood pressure as well as sodium and water homeostasis. However, local or paracrine RASs were later identified in many tissues, including in the brain. The tissue RAS basically consists of two arms, a pro-oxidative and pro-inflammatory axis in addition to an anti-oxidative and anti-inflammatory axis, that counteract each other to establish a correct balance in physiological conditions. The dysregulation of the tissue RAS is involved in different diseases and aging-related processes. In the brain, results from experimental models and clinical trials have involved the RAS in the progression of major neurodegenerative diseases such as Parkinson´s disease, Alzheimer’s disease, and other neurodegenerative processes via the promotion of oxidative stress and oxidative-stress-related mechanisms. Consistent with this, RAS-modulating drugs have been suggested as a possible neuroprotective strategy against the progression of neurodegeneration. 

We invite you to submit your latest research findings or a review article to this Special Issue, which will bring together current research concerning RAS and neurodegeneration. This Special Issue can include both clinical and experimental studies aiming to clarify possible mechanisms connecting the RAS and neurodegeneration as well as possible neuroprotective strategies based on RAS modulation.

We look forward to your contributions.

Prof. Dr. Jose L. Labandeira-Garcia
Dr. Ana I. Rodríguez-Pérez
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. 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

  • angiotensin
  • renin–angiotensin system
  • oxidative stress
  • neurodegeneration
  • neurodegenerative diseases
  • Parkinson’s
  • Alzheimer’s
  • neuroinflammation
  • neuroprotection

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Published Papers (3 papers)

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Research

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23 pages, 5659 KiB  
Article
Extracellular Vesicles and Their Renin–Angiotensin Cargo as a Link between Metabolic Syndrome and Parkinson’s Disease
by Maria A. Pedrosa, Carmen M. Labandeira, Nerea Lago-Baameiro, Rita Valenzuela, Maria Pardo, Jose Luis Labandeira-Garcia and Ana I. Rodriguez-Perez
Antioxidants 2023, 12(12), 2045; https://doi.org/10.3390/antiox12122045 - 26 Nov 2023
Cited by 5 | Viewed by 2391
Abstract
Several studies showed an association between metabolic syndrome (MetS) and Parkinson’s disease (PD). The linking mechanisms remain unclear. MetS promotes low-grade peripheral oxidative stress and inflammation and dysregulation of the adipose renin–angiotensin system (RAS). Interestingly, brain RAS dysregulation is involved in the progression [...] Read more.
Several studies showed an association between metabolic syndrome (MetS) and Parkinson’s disease (PD). The linking mechanisms remain unclear. MetS promotes low-grade peripheral oxidative stress and inflammation and dysregulation of the adipose renin–angiotensin system (RAS). Interestingly, brain RAS dysregulation is involved in the progression of dopaminergic degeneration and PD. Circulating extracellular vesicles (EVs) from MetS fat tissue can cross the brain–blood barrier and may act as linking signals. We isolated and characterized EVs from MetS and control rats and analyzed their mRNA and protein cargo using RT-PCR and the ExoView R200 platform, respectively. Furthermore, cultures of the N27 dopaminergic cell line and the C6 astrocytic cell line were treated with EVs from MetS rats. EVs were highly increased in MetS rat serum, which was inhibited by treatment of the rats with the angiotensin type-1-receptor blocker candesartan. Furthermore, EVs from MetS rats showed increased pro-oxidative/pro-inflammatory and decreased anti-oxidative/anti-inflammatory RAS components, which were inhibited in candesartan-treated MetS rats. In cultures, EVs from MetS rats increased N27 cell death and modulated C6 cell function, upregulating markers of neuroinflammation and oxidative stress, which were inhibited by the pre-treatment of cultures with candesartan. The results from rat models suggest EVs and their RAS cargo as a mechanism linking Mets and PD. Full article
(This article belongs to the Special Issue The Role of the Renin–Angiotensin System in Oxidative-Stress-Related Mechanisms in Neurodegenerative Diseases)
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22 pages, 3622 KiB  
Article
Interactions between Angiotensin Type-1 Antagonists, Statins, and ROCK Inhibitors in a Rat Model of L-DOPA-Induced Dyskinesia
by Andrea Lopez-Lopez, Rita Valenzuela, Ana Isabel Rodriguez-Perez, María J. Guerra, Jose Luis Labandeira-Garcia and Ana Muñoz
Antioxidants 2023, 12(7), 1454; https://doi.org/10.3390/antiox12071454 - 19 Jul 2023
Cited by 7 | Viewed by 2400
Abstract
Statins have been proposed for L-DOPA-induced dyskinesia (LID) treatment. Statin anti-dyskinetic effects were related to the inhibition of the Ras-ERK pathway. However, the mechanisms responsible for the anti-LID effect are unclear. Changes in cholesterol homeostasis and oxidative stress- and inflammation-related mechanisms such as [...] Read more.
Statins have been proposed for L-DOPA-induced dyskinesia (LID) treatment. Statin anti-dyskinetic effects were related to the inhibition of the Ras-ERK pathway. However, the mechanisms responsible for the anti-LID effect are unclear. Changes in cholesterol homeostasis and oxidative stress- and inflammation-related mechanisms such as angiotensin II and Rho-kinase (ROCK) inhibition may be involved. The nigra and striatum of dyskinetic rats showed increased levels of cholesterol, ROCK, and the inflammatory marker IL-1β, which were reduced by the angiotensin type-1 receptor (AT1) antagonist candesartan, simvastatin, and the ROCK inhibitor fasudil. As observed for LID, angiotensin II-induced, via AT1, increased levels of cholesterol and ROCK in the rat nigra and striatum. In cultured dopaminergic neurons, angiotensin II increased cholesterol biosynthesis and cholesterol efflux without changes in cholesterol uptake. In astrocytes, angiotensin induced an increase in cholesterol uptake, decrease in biosynthesis, and no change in cholesterol efflux, suggesting a neuronal accumulation of cholesterol that is reduced via transfer to astrocytes. Our data suggest mutual interactions between angiotensin/AT1, cholesterol, and ROCK pathways in LID, which are attenuated by the corresponding inhibitors. Interestingly, these three drugs have also been suggested as neuroprotective treatments against Parkinson’s disease. Therefore, they may reduce dyskinesia and the progression of the disease using common mechanisms. Full article
(This article belongs to the Special Issue The Role of the Renin–Angiotensin System in Oxidative-Stress-Related Mechanisms in Neurodegenerative Diseases)
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Review

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14 pages, 1218 KiB  
Review
The NADPH Link between the Renin Angiotensin System and the Antioxidant Mechanisms in Dopaminergic Neurons
by Rafael Franco, Joan Serrano-Marín, Gemma Navarro and Rafael Rivas-Santisteban
Antioxidants 2023, 12(10), 1869; https://doi.org/10.3390/antiox12101869 - 16 Oct 2023
Cited by 2 | Viewed by 2022
Abstract
The renin angiotensin system (RAS) has several components including signaling peptides, enzymes, and membrane receptors. The effort in characterizing this system in the periphery has led to the approval of a class of antihypertensives. Much less is known about RAS in the central [...] Read more.
The renin angiotensin system (RAS) has several components including signaling peptides, enzymes, and membrane receptors. The effort in characterizing this system in the periphery has led to the approval of a class of antihypertensives. Much less is known about RAS in the central nervous system. The production of RAS peptides and the expression of several RAS enzymes and receptors in dopaminergic neurons of the substantia nigra has raised expectations in the therapy of Parkinson’s disease, a neurodegenerative condition characterized by lack of dopamine in the striatum, the motor control region of the mammalian brain. On the one hand, dopamine production requires reducing power. On the other hand, reducing power is required by mechanisms involved in REDOX homeostasis. This review focuses on the potential role of RAS in the regulation of neuronal/glial expression of glucose-6-phosphate dehydrogenase, which produces the NADPH required for dopamine synthesis and for reactive oxygen species (ROS) detoxification. It is known that transgenic expression of the gene coding for glucose-6-phosphate dehydrogenase prevents the death of dopaminergic nigral neurons. Signaling via angiotensin II G protein-coupled receptors, AT1 or AT2, leads to the activation of protein kinase A and/or protein kinase C that in turn can regulate glucose-6- phosphate dehydrogenase activity, by Ser/Thr phosphorylation/dephosphorylation events. Long-term effects of AT1 or AT2 receptor activation may also impact on the concentration of the enzyme via activation of transcription factors that participate in the regulation of gene expression in neurons (or glia). Future research is needed to determine how the system can be pharmacologically manipulated to increase the availability of NADPH to neurons degenerating in Parkinson’s disease and to neuroprotective glia. Full article
(This article belongs to the Special Issue The Role of the Renin–Angiotensin System in Oxidative-Stress-Related Mechanisms in Neurodegenerative Diseases)
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