Renal expression of JAK2 is high in polycystic kidney disease and its inhibition reduces cystogenesis.

ABSTRACT: Autosomal dominant polycystic kidney disease (ADPKD) is the most common renal genetic disorder, however it still lacks a cure. The discovery of new therapies heavily depends on understanding key signalling pathways that lead to ADPKD. The JAnus Kinase and Signal Transducers and Activators of Transcription (JAK/STAT) pathway is aberrantly activated and contributes to ADPKD pathogenesis via enhancing epithelial proliferation. Yet the mechanisms underlying the upregulation of JAK/STAT activity in this disease context is completely unknown. Here, we investigate the role of JAK2 in ADPKD using a murine model of ADPKD (Pkd1^nl/nl). In normal kidneys, JAK2 expression is limited to tubular epithelial and vascular cells with lesser staining in bowman's capsule and remains below detection

SUBMITTER: Patera F 

PROVIDER: S-EPMC6418191 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature