Detrimental effects of hypoxia on glomerular podocytes.
| Title: | Detrimental effects of hypoxia on glomerular podocytes. |
|---|---|
| Authors: | Singh, Ashish K., Kolligundla, Lakshmi P., Francis, Justus, Pasupulati, Anil K. |
| Source: | Journal of Physiology & Biochemistry; May2021, Vol. 77 Issue 2, p193-203, 11p |
| Abstract: | Hypoxia-inducible factor1 (HIF1) plays a pivotal role in ensuring cells adapt to low-oxygen conditions. Depletion of oxygen, a co-substrate during hydroxylation of prolyl (P402 and P564) residues of HIF1⍺, evades HIF1⍺ ubiquitination and enables its dimerization with HIF1β to mediate global transcriptional response to hypoxia. Though HIF1 is largely considered eliciting a protective role during physiological or pathological hypoxia or ischemia, elevated HIF1 during chronic hypoxia contributes to glomerular diseases' pathology and proteinuria. The glomerulus is responsible for renal permselectivity and excretion of ultra-filtrated urine. Podocytes are the glomerulus' major cell types and are instrumental for glomerular filtration, permselectivity, and glomerular basement membrane maintenance. Podocyte injury is expected to impair the efficiency of glomerular filtration and manifestation of glomerulosclerosis and proteinuria. Accumulated evidence suggests that podocytes are susceptible to various insults during chronic hypoxia, including podocyte EMT, slit-diaphragm dysfunction, foot process effacement, and cytoskeletal derangement due to accumulation of HIF1. This review discusses how hypoxia/HIF1 signaling regulates various features and function of podocytes during exposure to chronic hypoxia or inducing HIF1 by various chemical modulators. [ABSTRACT FROM AUTHOR] |
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| Database: | Complementary Index |
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| Items | – Name: Title Label: Title Group: Ti Data: Detrimental effects of hypoxia on glomerular podocytes. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Singh%2C+Ashish+K%2E%22">Singh, Ashish K.</searchLink><br /><searchLink fieldCode="AR" term="%22Kolligundla%2C+Lakshmi+P%2E%22">Kolligundla, Lakshmi P.</searchLink><br /><searchLink fieldCode="AR" term="%22Francis%2C+Justus%22">Francis, Justus</searchLink><br /><searchLink fieldCode="AR" term="%22Pasupulati%2C+Anil+K%2E%22">Pasupulati, Anil K.</searchLink> – Name: TitleSource Label: Source Group: Src Data: Journal of Physiology & Biochemistry; May2021, Vol. 77 Issue 2, p193-203, 11p – Name: Abstract Label: Abstract Group: Ab Data: Hypoxia-inducible factor1 (HIF1) plays a pivotal role in ensuring cells adapt to low-oxygen conditions. Depletion of oxygen, a co-substrate during hydroxylation of prolyl (P402 and P564) residues of HIF1⍺, evades HIF1⍺ ubiquitination and enables its dimerization with HIF1β to mediate global transcriptional response to hypoxia. Though HIF1 is largely considered eliciting a protective role during physiological or pathological hypoxia or ischemia, elevated HIF1 during chronic hypoxia contributes to glomerular diseases' pathology and proteinuria. The glomerulus is responsible for renal permselectivity and excretion of ultra-filtrated urine. Podocytes are the glomerulus' major cell types and are instrumental for glomerular filtration, permselectivity, and glomerular basement membrane maintenance. Podocyte injury is expected to impair the efficiency of glomerular filtration and manifestation of glomerulosclerosis and proteinuria. Accumulated evidence suggests that podocytes are susceptible to various insults during chronic hypoxia, including podocyte EMT, slit-diaphragm dysfunction, foot process effacement, and cytoskeletal derangement due to accumulation of HIF1. This review discusses how hypoxia/HIF1 signaling regulates various features and function of podocytes during exposure to chronic hypoxia or inducing HIF1 by various chemical modulators. [ABSTRACT FROM AUTHOR] – Name: Abstract Label: Group: Ab Data: <i>Copyright of Journal of Physiology & Biochemistry is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1007/s13105-021-00788-y Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 11 StartPage: 193 Titles: – TitleFull: Detrimental effects of hypoxia on glomerular podocytes. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Singh, Ashish K. – PersonEntity: Name: NameFull: Kolligundla, Lakshmi P. – PersonEntity: Name: NameFull: Francis, Justus – PersonEntity: Name: NameFull: Pasupulati, Anil K. IsPartOfRelationships: – BibEntity: Dates: – D: 01 M: 05 Text: May2021 Type: published Y: 2021 Identifiers: – Type: issn-print Value: 11387548 Numbering: – Type: volume Value: 77 – Type: issue Value: 2 Titles: – TitleFull: Journal of Physiology & Biochemistry Type: main |
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