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Status: Bibliographieeintrag

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Verfasst von:Ott, Hannes [VerfasserIn]   i
 Bennewitz, Katrin [VerfasserIn]   i
 Zhang, Xin [VerfasserIn]   i
 Prianichnikova, Mariia [VerfasserIn]   i
 Sticht, Carsten [VerfasserIn]   i
 Poschet, Gernot [VerfasserIn]   i
 Kroll, Jens [VerfasserIn]   i
Titel:Sodium thiosulfate treatment rescues hyperglycaemia-induced pronephros damage in zebrafish by upregulating nitric oxide signalling
Verf.angabe:Hannes Ott, Katrin Bennewitz, Xin Zhang, Mariia Prianichnikova, Carsten Sticht, Gernot Poschet and Jens Kroll
Jahr:2024
Umfang:14 S.
Illustrationen:Illustrationen
Fussnoten:Online veröffentlicht: 12. September 2024 ; Gesehen am 27.01.2024
Titel Quelle:Enthalten in: The journal of physiology
Ort Quelle:Hoboken, NJ : Wiley-Blackwell, 1878
Jahr Quelle:2024
Band/Heft Quelle:(2024), Seite 1-14
ISSN Quelle:1469-7793
Abstract:Sodium thiosulfate (STS) is gaining increasing attention in research for its potential therapeutic applications across a spectrum of disease processes beyond its current uses. However, the precise mechanisms of action remain incompletely understood. We investigated the efficacy of STS in treating hyperglycaemia-induced pronephros damage in zebrafish to gain further insight into the underlying mechanisms. Hyperglycaemia was induced in zebrafish by suppressing the pdx1 transcription factor, which plays a crucial role in maintaining physiological pancreatic function. STS was administered by introducing it into the medium of zebrafish larvae. The pronephros structure was analysed at 48 h post-fertilization. Metabolomic profiling and RNA sequencing were conducted on groups exposed to various experimental conditions. Our findings reveal a downregulation of nitric oxide (NO) signalling in zebrafish with a knocked-down pdx1 gene, both metabolomically and transcriptionally. Notably, treatment with STS led to a compensatory upregulation of the NO signalling, ultimately resulting in the rescue of the pronephros structure. Our study provides compelling evidence that targeting NO metabolism by the administration of STS offers a promising strategy for addressing hyperglycaemia-induced organ damage. These findings underscore the potential of STS as a promising therapeutic agent for diabetic complications and warrant further investigation of its clinical applications. Key points Sodium thiosulfate (STS) is increasingly drawing attention in research for its potential therapeutic applications across a spectrum of disease processes. Here, we demonstrate that STS treatment rescues hyperglycaemia-induced pronephros damage in zebrafish. We identified upregulation of nitric oxide signalling as the major driver behind STS-mediated rescue. Our data suggest that STS offers a promising strategy for addressing hyperglycaemia-induced organ damage, including diabetic nephropathy.
DOI:doi:10.1113/JP286398
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

kostenfrei: Volltext: https://doi.org/10.1113/JP286398
 kostenfrei: Volltext: http://onlinelibrary.wiley.com/doi/abs/10.1113/JP286398
 DOI: https://doi.org/10.1113/JP286398
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:diabetes mellitus
 nitric oxide
 sodium thiosulfate
 zebrafish
K10plus-PPN:1915616735
Verknüpfungen:→ Zeitschrift

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