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Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases
Brain neurodegenerative diseases (BND) are debilitating conditions that are especially characteristic of a certain period of life and considered major threats to human health. Current treatments are limited, meaning that there is a challenge in developing new options that can efficiently tackle the...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9599929/ https://www.ncbi.nlm.nih.gov/pubmed/36291638 http://dx.doi.org/10.3390/biom12101429 |
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author | Bild, Walther Vasincu, Alexandru Rusu, Răzvan-Nicolae Ababei, Daniela-Carmen Stana, Aurelian Bogdan Stanciu, Gabriela Dumitrița Savu, Bogdan Bild, Veronica |
author_facet | Bild, Walther Vasincu, Alexandru Rusu, Răzvan-Nicolae Ababei, Daniela-Carmen Stana, Aurelian Bogdan Stanciu, Gabriela Dumitrița Savu, Bogdan Bild, Veronica |
author_sort | Bild, Walther |
collection | PubMed |
description | Brain neurodegenerative diseases (BND) are debilitating conditions that are especially characteristic of a certain period of life and considered major threats to human health. Current treatments are limited, meaning that there is a challenge in developing new options that can efficiently tackle the different components and pathophysiological processes of these conditions. The renin-angiotensin-aldosterone system (RAS) is an endocrine axis with important peripheral physiological functions such as blood pressure and cardiovascular homeostasis, as well as water and sodium balance and systemic vascular resistance—functions which are well-documented. However, recent work has highlighted the paracrine and autocrine functions of RAS in different tissues, including the central nervous system (CNS). It is known that RAS hyperactivation has pro-inflammatory and pro-oxidant effects, thus suggesting that its pharmacological modulation could be used in the management of these conditions. The present paper underlines the involvement of RAS and its components in the pathophysiology of BNDs such as Parkinson’s disease (PD), Alzheimer’s disease (AD), multiple sclerosis (MS), Huntington’s disease (HD), motor neuron disease (MND), and prion disease (PRD), as well as the identification of drugs and pharmacologically active substances that act upon RAS, which could alleviate their symptomatology or evolution, and thus, contribute to novel therapeutic approaches. |
format | Online Article Text |
id | pubmed-9599929 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-95999292022-10-27 Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases Bild, Walther Vasincu, Alexandru Rusu, Răzvan-Nicolae Ababei, Daniela-Carmen Stana, Aurelian Bogdan Stanciu, Gabriela Dumitrița Savu, Bogdan Bild, Veronica Biomolecules Review Brain neurodegenerative diseases (BND) are debilitating conditions that are especially characteristic of a certain period of life and considered major threats to human health. Current treatments are limited, meaning that there is a challenge in developing new options that can efficiently tackle the different components and pathophysiological processes of these conditions. The renin-angiotensin-aldosterone system (RAS) is an endocrine axis with important peripheral physiological functions such as blood pressure and cardiovascular homeostasis, as well as water and sodium balance and systemic vascular resistance—functions which are well-documented. However, recent work has highlighted the paracrine and autocrine functions of RAS in different tissues, including the central nervous system (CNS). It is known that RAS hyperactivation has pro-inflammatory and pro-oxidant effects, thus suggesting that its pharmacological modulation could be used in the management of these conditions. The present paper underlines the involvement of RAS and its components in the pathophysiology of BNDs such as Parkinson’s disease (PD), Alzheimer’s disease (AD), multiple sclerosis (MS), Huntington’s disease (HD), motor neuron disease (MND), and prion disease (PRD), as well as the identification of drugs and pharmacologically active substances that act upon RAS, which could alleviate their symptomatology or evolution, and thus, contribute to novel therapeutic approaches. MDPI 2022-10-06 /pmc/articles/PMC9599929/ /pubmed/36291638 http://dx.doi.org/10.3390/biom12101429 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Bild, Walther Vasincu, Alexandru Rusu, Răzvan-Nicolae Ababei, Daniela-Carmen Stana, Aurelian Bogdan Stanciu, Gabriela Dumitrița Savu, Bogdan Bild, Veronica Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases |
title | Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases |
title_full | Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases |
title_fullStr | Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases |
title_full_unstemmed | Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases |
title_short | Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases |
title_sort | impact of the renin-angiotensin system on the pathogeny and pharmacotherapeutics of neurodegenerative diseases |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9599929/ https://www.ncbi.nlm.nih.gov/pubmed/36291638 http://dx.doi.org/10.3390/biom12101429 |
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