Lack of APOL1 in proximal tubules of normal human kidneys and proteinuric APOL1 transgenic mouse kidneys.

The mechanism of pathogenesis associated with APOL1 polymorphisms and risk for non-diabetic chronic kidney disease (CKD) is not fully understood. Prior studies have minimized a causal role for the circulating APOL1 protein, thus efforts to understand kidney pathogenesis have focused on APOL1 express...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Natalya A Blessing, Zhenzhen Wu, Sethu M Madhavan, Jonathan W Choy, Michelle Chen, Myung K Shin, Maarten Hoek, John R Sedor, John F O'Toole, Leslie A Bruggeman
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2021
Materias:
R
Q
Acceso en línea:https://doaj.org/article/fd5027d0c5714bc48fd1f7b797f2cb73
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!