Automated Organization ProfileIII. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany 2Hamburg Center for Kidney Health (HCKH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany
III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany 2Hamburg Center for Kidney Health (HCKH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Current S-Index
Sum of Dataset Indices for all datasets
Average Dataset Index per Dataset
Average Dataset Index per dataset
Total Datasets
Total datasets in this organization
Average FAIR Score
Average FAIR Score per dataset
Total Citations
Total citations to the organization's datasets
Total Mentions
Total mentions of the organization's datasets
S-Index Interpretation
The S-Index (Sharing Index) is a comprehensive metric that represents the cumulative impact of all your datasets. It is calculated as the sum of Dataset Index scores across all your claimed datasets.
What it means:
- A higher S-index indicates greater overall impact of your datasets relative to typical datasets in their fields of research
- The S-Index grows as you add more datasets or as existing datasets gain more citations and mentions
- It provides a single number to track your research data impact over time
Current S-Index: 0.0 (sum of 2 datasets Dataset Index scores)
More information here.
S-Index Over Time
Cumulative Citations Over Time
Cumulative Mentions Over Time
Datasets
Low nephron endowment constitutes a risk factor for hypertension and renal disease. Epigenetic regulation is crucial for nephron progenitor cell differentiation, impacting nephron number and renal function. The role of many epigenetic modulators, such as Lysine-specific histone demethylase 1a (LSD1), remains unclear. We used Lsd1 knockout mice to demonstrate that Lsd1 depletion in nephron progenitor cells results in reduced kidney size in neonates and leads to glomerulosclerosis, proteinuria, and renal cysts in adults. Notably, LSD1 deletion in podocytes or tubular cells did not replicate these effects. CRISPR/Cas9-mediated LSD1 deletion in human kidney organoids caused cyst formation and altered gene expression, with snRNA-seq revealing downregulation of podocyte genes and upregulation of metabolic genes. The presence of non-coding RNAs indicates roles in cell proliferation. Our study reveals the critical role of LSD1 function in nephron development and highlights its impact on transcriptional programming for long-term renal function and susceptibility to cyst formation.
Authors
- Wanner, Nicola ;
- Liaukouskaya, Nastassia ;
- Gies, Sydney E. ;
- Andrieux, Geoffroy ;
- Huber, Tobias B.
Low nephron endowment constitutes a risk factor for hypertension and renal disease. Epigenetic regulation is crucial for nephron progenitor cell differentiation, impacting nephron number and renal function. The role of many epigenetic modulators, such as Lysine-specific histone demethylase 1a (LSD1), remains unclear. We used Lsd1 knockout mice to demonstrate that Lsd1 depletion in nephron progenitor cells results in reduced kidney size in neonates and leads to glomerulosclerosis, proteinuria, and renal cysts in adults. Notably, LSD1 deletion in podocytes or tubular cells did not replicate these effects. CRISPR/Cas9-mediated LSD1 deletion in human kidney organoids caused cyst formation and altered gene expression, with snRNA-seq revealing downregulation of podocyte genes and upregulation of metabolic genes. The presence of non-coding RNAs indicates roles in cell proliferation. Our study reveals the critical role of LSD1 function in nephron development and highlights its impact on transcriptional programming for long-term renal function and susceptibility to cyst formation.
Authors
- Wanner, Nicola ;
- Liaukouskaya, Nastassia ;
- Gies, Sydney E. ;
- Andrieux, Geoffroy ;
- Huber, Tobias B.