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...
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Autores principales: | , , , , , , , , , |
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Formato: | article |
Lenguaje: | EN |
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Public Library of Science (PLoS)
2021
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Acceso en línea: | https://doaj.org/article/fd5027d0c5714bc48fd1f7b797f2cb73 |
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