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- W3089984307 abstract "Defective recycling of megalin consequent to impaired phosphatidylinositol metabolism has been implicated as a mechanism causing tubular proteinuria in patients with Lowe syndrome. In this issue, Berquez et al. describe an innovative approach using a clinically approved drug to “rebalance” phosphatidylinositols and restore megalin traffic in mouse and cell models of the disease. Defective recycling of megalin consequent to impaired phosphatidylinositol metabolism has been implicated as a mechanism causing tubular proteinuria in patients with Lowe syndrome. In this issue, Berquez et al. describe an innovative approach using a clinically approved drug to “rebalance” phosphatidylinositols and restore megalin traffic in mouse and cell models of the disease. The phosphoinositide 3-kinase inhibitor alpelisib restores actin organization and improves proximal tubule dysfunction in vitro and in a mouse model of Lowe syndrome and Dent diseaseKidney InternationalVol. 98Issue 4PreviewLoss-of-function mutations in the OCRL gene, which encodes the phosphatidylinositol [PI] 4,5-bisphosphate [PI(4,5)P2] 5-phosphatase OCRL, cause defective endocytosis and proximal tubule dysfunction in Lowe syndrome and Dent disease 2. The defect is due to increased levels of PI(4,5)P2 and aberrant actin polymerization, blocking endosomal trafficking. PI 3-phosphate [PI(3)P] has been recently identified as a coactivator with PI(4,5)P2 in the actin pathway. Here, we tested the hypothesis that phosphoinositide 3-kinase (PI3K) inhibitors may rescue the endocytic defect imparted by OCRL loss, by rebalancing phosphoinositide signals to the actin machinery. Full-Text PDF Open Access" @default.
- W3089984307 created "2020-10-08" @default.
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- W3089984307 date "2020-10-01" @default.
- W3089984307 modified "2023-10-14" @default.
- W3089984307 title "Targeting PIs to improve PTs:a new approach to treating genetic diseases of the proximal tubule" @default.
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- W3089984307 doi "https://doi.org/10.1016/j.kint.2020.06.018" @default.
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