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Tubular STAT3 limits renal inflammation in autosomal dominant polycystic kidney disease
[article]
2019
bioRxiv
pre-print
ABSTRACTThe inactivation of the ciliary proteins polycystin 1 or 2 leads to autosomal dominant polycystic kidney disease (ADPKD), the leading genetic cause of chronic kidney disease. Both cilia signaling and interstitial inflammation play a critical role in the disease. Yet, the reciprocal interactions between immune and tubular cells are not well characterized. The transcription factor STAT3, which is suspected to fuel ADPKD progression, is involved in crosstalks between immune and non-immune
doi:10.1101/2019.12.12.873901
fatcat:pcriabfqkfcabkrzswgpnk5wyy