Polycystic kidney is a debilitating condition observed in several genetic diseases, including Ciliopathies, Autosomal Dominant Polycystic Kidney Disease (ADPKD) and Tuberous Sclerosis Complex. This disorder is accompanied by the activation of the mammalian Target Of Rapamycin (mTOR) pathway, a master regulator of the growth responses within the cell. In a Nature Communications article published in June 2020, three research groups at Inem shed new light on how mTOR may lead to polycystic kidney. Using cellular and animal models of Tuberous Sclerosis Complex, the Pende group in collaboration with the Terzi and Pontoglio teams demonstrates that mTOR not only promotes cell growth and proliferation but also regulates oriented cell division. They provide evidence that, when mTOR activity is uncontrolled, kidney epithelial cells do not proliferate anymore along the tubular axis but in a distorted way leading to tubule enlargement rather than elongation. The molecular players may become new therapeutic targets.
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