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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...

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Autores principales: Semenikhina, Marharyta, Stefanenko, Mariia, Spires, Denisha R., Ilatovskaya, Daria V., Palygin, Oleg
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
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.
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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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