A research team from the Department of Internal Medicine D – Geriatrics at the University Medical Center Greifswald has made significant progress in understanding chronic kidney disease in a recent study. The scientists investigated the effect of a special ion channel, TRPC6, and discovered a new cell type that could regulate inflammation and prevent the development of renal fibrosis. The results, published in the journal Advanced Science, open up new perspectives for targeted therapies for chronic kidney disease, which affects millions of people worldwide and often requires dialysis or transplantation.

The study focused on the TRPC6 ion channel, which is found in the kidneys. Mutations of this channel can trigger focal segmental glomerulosclerosis (FSGS), a form of chronic kidney disease. The Greifswald researchers used a substance called SH045, obtained from European larch, to inhibit TRPC6 in mice with kidney damage. This treatment protects the kidney from damage and scarring. Using state-of-the-art single-cell gene analysis (single-cell RNA sequencing), the scientists examined around 20,000 kidney cells to analyze changes in various cell types such as inflammatory cells, endothelial cells or fibroblasts. They identified a previously unknown cell type that regulates inflammation and was also detected in human kidney biopsies.

The findings are a breakthrough in understanding the complex mechanisms of kidney disease, particularly in old age. They could form the basis for new, more effective therapies with fewer side effects. By specifically modulating TRPC6, future treatments could slow down or stop the progression of renal fibrosis. Current treatment options for chronic kidney disease are limited and often associated with severe side effects. The Greifswald research thus shows a promising path for the development of innovative drugs that offer patients new hope.

Original Paper:

Single-Cell RNA Sequencing Delineates Renal Anti-Fibrotic Mechanisms Mediated by TRPC6 Inhibition – Xu – Advanced Science – Wiley Online Library

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