![[feed]](/style/images/feed-icon-14x14.png){kind=icon}
Tools
Tools
Preview |
PDF (Original Article)
- Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader
16MB |
![[thumbnail of Supplementary Information]](https://edoc.mdc-berlin.de/style/images/fileicons/other.png) |
Other (Supplementary Information)
10MB |
| Item Type: | Article |
|---|---|
| Title: | Role of TRPC6 in kidney damage after acute ischemic kidney injury |
| Creators Name: | Zheng, Z., Tsvetkov, D., Bartolomaeus, T.U.P., Erdogan, C., Krügel, U., Schleifenbaum, J., Schaefer, M., Nürnberg, B., Chai, X., Ludwig, F.A., N'diaye, G., Köhler, M.B., Wu, K., Gollasch, M. and Markó, L. |
| Abstract: | Transient receptor potential channel subfamily C, member 6 (TRPC6), a non-selective cation channel that controls influx of Ca(2+) and other monovalent cations into cells, is widely expressed in the kidney. TRPC6 gene variations have been linked to chronic kidney disease but its role in acute kidney injury (AKI) is unknown. Here we aimed to investigate the putative role of TRPC6 channels in AKI. We used Trpc6(-/-) mice and pharmacological blockade (SH045 and BI-749327), to evaluate short-term AKI outcomes. Here, we demonstrate that neither Trpc6 deficiency nor pharmacological inhibition of TRPC6 influences the short-term outcomes of AKI. Serum markers, renal expression of epithelial damage markers, tubular injury, and renal inflammatory response assessed by the histological analysis were similar in wild-type mice compared to Trpc6(-/-) mice as well as in vehicle-treated versus SH045- or BI-749327-treated mice. In addition, we also found no effect of TRPC6 modulation on renal arterial myogenic tone by using blockers to perfuse isolated kidneys. Therefore, we conclude that TRPC6 does not play a role in the acute phase of AKI. Our results may have clinical implications for safety and health of humans with TRPC6 gene variations, with respect to mutated TRPC6 channels in the response of the kidney to acute ischemic stimuli. |
| Keywords: | APACHE, Acute Kidney Injury, Calcium, Genetic Variation, Ischemia, Kidney, Negative Results, TRPC6 Cation Channel, TRPC6 Cation Channel / Physiology, Transgenic Mice, Animals, Mice |
| Source: | Scientific Reports |
| ISSN: | 2045-2322 |
| Publisher: | Nature Publishing Group |
| Volume: | 12 |
| Number: | 1 |
| Page Range: | 3038 |
| Date: | 22 February 2022 |
| Official Publication: | https://doi.org/10.1038/s41598-022-06703-9 |
| PubMed: | View item in PubMed |
Repository Staff Only: item control page
