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Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology
Nitric oxide (NO) is a potent signaling molecule involved in many physiological and pathophysiological processes in the kidney. NO plays a complex role in glomerular ultrafiltration, vasodilation, and inflammation. Changes in NO bioavailability in pathophysiological conditions such as hypertension o...
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/PMC9221338/ https://www.ncbi.nlm.nih.gov/pubmed/35740870 http://dx.doi.org/10.3390/biom12060745 |
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author | Semenikhina, Marharyta Stefanenko, Mariia Spires, Denisha R. Ilatovskaya, Daria V. Palygin, Oleg |
author_facet | Semenikhina, Marharyta Stefanenko, Mariia Spires, Denisha R. Ilatovskaya, Daria V. Palygin, Oleg |
author_sort | Semenikhina, Marharyta |
collection | PubMed |
description | Nitric oxide (NO) is a potent signaling molecule involved in many physiological and pathophysiological processes in the kidney. NO plays a complex role in glomerular ultrafiltration, vasodilation, and inflammation. Changes in NO bioavailability in pathophysiological conditions such as hypertension or diabetes may lead to podocyte damage, proteinuria, and rapid development of chronic kidney disease (CKD). Despite the extensive data highlighting essential functions of NO in health and pathology, related signaling in glomerular cells, particularly podocytes, is understudied. Several reports indicate that NO bioavailability in glomerular cells is decreased during the development of renal pathology, while restoring NO level can be beneficial for glomerular function. At the same time, the compromised activity of nitric oxide synthase (NOS) may provoke the formation of peroxynitrite and has been linked to autoimmune diseases such as systemic lupus erythematosus. It is known that the changes in the distribution of NO sources due to shifts in NOS subunits expression or modifications of NADPH oxidases activity may be linked to or promote the development of pathology. However, there is a lack of information about the detailed mechanisms describing the production and release of NO in the glomerular cells. The interaction of NO and other reactive oxygen species in podocytes and how NO-calcium crosstalk regulates glomerular cells’ function is still largely unknown. Here, we discuss recent reports describing signaling, synthesis, and known pathophysiological mechanisms mediated by the changes in NO homeostasis in the podocyte. The understanding and further investigation of these essential mechanisms in glomerular cells will facilitate the design of novel strategies to prevent or manage health conditions that cause glomerular and kidney damage. |
format | Online Article Text |
id | pubmed-9221338 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-92213382022-06-24 Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology Semenikhina, Marharyta Stefanenko, Mariia Spires, Denisha R. Ilatovskaya, Daria V. Palygin, Oleg Biomolecules Review Nitric oxide (NO) is a potent signaling molecule involved in many physiological and pathophysiological processes in the kidney. NO plays a complex role in glomerular ultrafiltration, vasodilation, and inflammation. Changes in NO bioavailability in pathophysiological conditions such as hypertension or diabetes may lead to podocyte damage, proteinuria, and rapid development of chronic kidney disease (CKD). Despite the extensive data highlighting essential functions of NO in health and pathology, related signaling in glomerular cells, particularly podocytes, is understudied. Several reports indicate that NO bioavailability in glomerular cells is decreased during the development of renal pathology, while restoring NO level can be beneficial for glomerular function. At the same time, the compromised activity of nitric oxide synthase (NOS) may provoke the formation of peroxynitrite and has been linked to autoimmune diseases such as systemic lupus erythematosus. It is known that the changes in the distribution of NO sources due to shifts in NOS subunits expression or modifications of NADPH oxidases activity may be linked to or promote the development of pathology. However, there is a lack of information about the detailed mechanisms describing the production and release of NO in the glomerular cells. The interaction of NO and other reactive oxygen species in podocytes and how NO-calcium crosstalk regulates glomerular cells’ function is still largely unknown. Here, we discuss recent reports describing signaling, synthesis, and known pathophysiological mechanisms mediated by the changes in NO homeostasis in the podocyte. The understanding and further investigation of these essential mechanisms in glomerular cells will facilitate the design of novel strategies to prevent or manage health conditions that cause glomerular and kidney damage. MDPI 2022-05-25 /pmc/articles/PMC9221338/ /pubmed/35740870 http://dx.doi.org/10.3390/biom12060745 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 Semenikhina, Marharyta Stefanenko, Mariia Spires, Denisha R. Ilatovskaya, Daria V. Palygin, Oleg Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology |
title | Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology |
title_full | Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology |
title_fullStr | Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology |
title_full_unstemmed | Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology |
title_short | Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology |
title_sort | nitric-oxide-mediated signaling in podocyte pathophysiology |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9221338/ https://www.ncbi.nlm.nih.gov/pubmed/35740870 http://dx.doi.org/10.3390/biom12060745 |
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