Pkd2 Deficiency in Embryonic Aqp2+ Progenitor Cells Is Sufficient to Cause Severe Polycystic Kidney Disease.
Akaki TsilosaniChao GaoEnuo ChenAndrea R LightleSana ShehzadMadhulika SharmaPamela V TranCarlton Matthew BatesDarren P WallaceWenzheng ZhangPublished in: Journal of the American Society of Nephrology : JASN (2024)
Hence, Pkd2 deletion in embryonic AP, but unlikely in neonate or adult Aqp2+ cells (PC and AP), was sufficient to cause severe PKD with progressive elimination of α-IC, recapitulating a newly identified cellular phenotype of ADPKD patients. We proposed that Pkd2 is critical for balanced AP differentiation into, proliferation and/or maintenance of cystic IC, particularly α-IC.
Keyphrases
- polycystic kidney disease
- transcription factor
- end stage renal disease
- ejection fraction
- induced apoptosis
- newly diagnosed
- chronic kidney disease
- early onset
- signaling pathway
- multiple sclerosis
- prognostic factors
- peritoneal dialysis
- cell cycle arrest
- oxidative stress
- drug induced
- patient reported outcomes
- cell death
- young adults