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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| Formáid: | Alt |
| Teanga: | English |
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MDPI AG
2022-05-01
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| Sraith: | Biomolecules |
| Ábhair: | |
| Rochtain ar líne: | https://www.mdpi.com/2218-273X/12/6/745 |
| _version_ | 1827662006804545536 |
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| author | Marharyta Semenikhina Mariia Stefanenko Denisha R. Spires Daria V. Ilatovskaya Oleg Palygin |
| author_facet | Marharyta Semenikhina Mariia Stefanenko Denisha R. Spires Daria V. Ilatovskaya Oleg Palygin |
| author_sort | Marharyta Semenikhina |
| collection | DOAJ |
| 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. |
| first_indexed | 2024-03-10T00:19:06Z |
| format | Article |
| id | doaj.art-970e901b483146f2a28f84752b7eeb57 |
| institution | Directory Open Access Journal |
| issn | 2218-273X |
| language | English |
| last_indexed | 2024-03-10T00:19:06Z |
| publishDate | 2022-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomolecules |
| spelling | doaj.art-970e901b483146f2a28f84752b7eeb572023-11-23T15:46:11ZengMDPI AGBiomolecules2218-273X2022-05-0112674510.3390/biom12060745Nitric-Oxide-Mediated Signaling in Podocyte PathophysiologyMarharyta Semenikhina0Mariia Stefanenko1Denisha R. Spires2Daria V. Ilatovskaya3Oleg Palygin4Division of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USADivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USADepartment of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USADepartment of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USADivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USANitric 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.https://www.mdpi.com/2218-273X/12/6/745nitric oxide synthaseglomeruluslupus nephritishypertension |
| spellingShingle | Marharyta Semenikhina Mariia Stefanenko Denisha R. Spires Daria V. Ilatovskaya Oleg Palygin Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology Biomolecules nitric oxide synthase glomerulus lupus nephritis hypertension |
| 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 | nitric oxide synthase glomerulus lupus nephritis hypertension |
| url | https://www.mdpi.com/2218-273X/12/6/745 |
| work_keys_str_mv | AT marharytasemenikhina nitricoxidemediatedsignalinginpodocytepathophysiology AT mariiastefanenko nitricoxidemediatedsignalinginpodocytepathophysiology AT denisharspires nitricoxidemediatedsignalinginpodocytepathophysiology AT dariavilatovskaya nitricoxidemediatedsignalinginpodocytepathophysiology AT olegpalygin nitricoxidemediatedsignalinginpodocytepathophysiology |