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Vascular mechanism of kidney disease

​Diabetic nephropathy (dNP) is the leading cause of end-stage renal disease worldwide. Glomerular filtration barrier disruption as well as tubular cell injury contributes to the pathogenesis of dNP. Coagulation proteases have been shown to play a role in dNP. In this regard, our group has previously shown that activated protein C can convey cytoprotective effects via protease activated receptor (PAR) signaling in the kidney independent of its anti-coagulant effects. Furthermore, we have studied the involvement of several cytodisruptive mechanisms such as the activation of the inflammasome, ER-stress and cellular proteostasis in acute as well as chronic kidney injury.

The focus of current projects in the group is to study the involvement of different coagulation regulators in regulating cellular function in different renal cells within the kidney. We aim to study these cellular mechanisms within the glomerular as well as tubular compartment. Particularly, we aim to study the mechanisms regulating the glomerular barrier disruption, tubular injury and tubular regeneration using acute as well as chronic kidney injury mouse models. Furthermore, we are using state of the art techniques such as sea-horse, cell lineage tracing, live-cell imaging, microfluidics and omics studies such as single cell RNA sequencing, metabolomics and proteomics to identify novel mechanisms regulating cellular pathways within the kidney.

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