The kidney removes waste, water and solute from the body to maintain a constant composition of the fluid that bathes our cells (i.e., homeostasis). To do so, the kidney filters around 180 litres of plasma each day through the glomeruli. This filtrate then enters kidney tubules, which reabsorbed molecules that need to be retained to achieve homeostasis, thereby concentrating unwanted wastes in the final urine. The tubular cells are equipped with an antennae-like structure called “the primary cilium”, which is in direct contact with the forming urine and is sought to sense mechanical and chemical cues derived from the urinary flow. Mutations affecting ciliary genes are the leading causes of genetic kidney failure. They can cause a cystic transformation of kidney tubules (as in Autosomal Dominant Polycystic Kidney Disease; ADPKD) or a progressive fibro-inflammatory destruction of the kidney. These diseases pinpoint cilia as crucial gate keepers of kidney architecture but the mechanisms involved remained unclear. The aim of my team is to provide novel therapies for patients suffering from cilia-related kidney diseases through a better understanding of the function of cilia in kidney maintenance.

We focus our research on the role of cilia in (i) adapting kidney cells to mechanical constraints and (ii) regulating inflammatory and scarring responses to damage and/or pathogens. To this aim, we use complex genetic animal models, cell culture and patients derived material.

In addition, we have developed fruitful collaboration with a bunch of fantastic researchers working in complementary fields including biophysicists, physiologists, geneticists, immunologists and bacteriologists.