Kai Martin Schmidt-Ott

AVPR2 antagonism with tolvaptan alters medullary cell responses and attenuates kidney injury

This study shows that Tolvaptan reduces medullary cell stress and inflammation in kidney injury models.

Canonical Notch2 Signaling Regulates the Development of Iron-recycling Macrophages and Iron Homeostasis

Cyst-type epithelial heterogeneity shapes therapeutic responsiveness in ADPKD

The paper identifies three epithelial cyst types in ADPKD using single-nucleus RNA sequencing and machine learning, showing their association with therapeutic response.

Macrophages induce stromal differentiation and endothelialization in iPSC-derived kidney organoids.

This study shows that macrophages induce endothelial and stromal differentiation in kidney organoids, enhancing vascularization and maturation.

Interleukin enhancer binding factor 2 (Ilf2) and kidney epithelial stress resilience

This study identifies Ilf2 as a key regulator of kidney epithelial stress resilience through transcriptional and splicing programs in cultured cells and mouse models.

Discovery of a non-canonical GRHL1 binding site using deep convolutional and recurrent neural networks

The paper uses deep learning to identify non-canonical GRHL1 binding sites not detected by traditional PWM methods.

The centrosomal protein 83 (CEP83) regulates human pluripotent stem cell differentiation towards the kidney lineage

This study shows that CEP83 deficiency in hiPSCs disrupts intermediate mesoderm differentiation, leading to impaired kidney progenitor formation and increased LPM marker expression.

Urinary single-cell sequencing captures intrarenal injury and repair processes in human acute kidney injury

This study uses urinary single-cell RNA sequencing to analyze injury and repair processes in acute kidney injury, identifying distinct cellular and molecular dynamics.

Transcriptomic responses of the human kidney to acute injury at single cell resolution

This study uses single-nuclei transcriptomics to analyze human kidney injury responses, identifying four injury-associated cell states and showing similar gene expression changes between AKI patients with and without COVID-19.