ReviewClinical and experimental nephrology2018
Activation of AQP2 water channels without vasopressin: therapeutic strategies for congenital nephrogenic diabetes insipidus.
Review in Clinical and experimental nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- The hidden players: LncRNA-Encoded micropeptides in cancer hallmarks.Cellular and molecular life sciences : CMLS · 2026Review
- Wnt-5a ameliorates sepsis-induced downregulation of renal AQP2 via the calcineurin signaling pathway.Clinical and experimental nephrology · 2025Article
- Construction of arginine vasopressin receptor 2-deficient rats by the rGONAD method.Clinical and experimental nephrology · 2025Article
- Exploring the diversity of AVPR2 in Primates and its evolutionary implications.Genetics and molecular biology · 2023Article
- Congenital nephrogenic diabetes insipidus arginine vasopressin receptor 2 gene mutation at new site: A case report.World journal of clinical cases · 2022Article
- Micropeptide MIAC inhibits the tumor progression by interacting with AQP2 and inhibiting EREG/EGFR signaling in renal cell carcinoma.Molecular cancer · 2022Article
- Activation of AQP2 water channels by protein kinase A: therapeutic strategies for congenital nephrogenic diabetes insipidus.Clinical and experimental nephrology · 2021Review
- Nephrogenic diabetes insipidus in children (Review).Experimental and therapeutic medicine · 2021Review
- Functional characterization of a loss-of-function mutant I324M of arginine vasopressin receptor 2 in X-linked nephrogenic diabetes insipidus.Scientific reports · 2021Article
- The long-term effects of rapamycin-based immunosuppressive protocols on the expression of renal aquaporins 1, 2, 3 and 4 water channels in rats.Histology and histopathology · 2021Article
- Case Report: A Case of Congenital Nephrogenic Diabetes Insipidus Caused by Thr273Met Mutation in Arginine Vasopressin Receptor 2.Frontiers in pediatrics · 2021Article
- Congenital nephrogenic diabetes insipidus due to the mutation inWorld journal of clinical cases · 2020Article
- Nephrogenic diabetes insipidus induced by ureter obstruction due to benign prostatic hyperplasia: A case report.Medicine · 2020Article
- Targeting the Trafficking of Kidney Water Channels for Therapeutic Benefit.Annual review of pharmacology and toxicology · 2020Review
- Tolvaptan activates the Nrf2/HO-1 antioxidant pathway through PERK phosphorylation.Scientific reports · 2019Article
- An Antifungal for Antidiuresis?Journal of the American Society of Nephrology : JASN · 2019Article
- Vasopressin-Independent Regulation of Aquaporin-2 by Tamoxifen in Kidney Collecting Ducts.Frontiers in physiology · 2019Article
- Vasopressin-aquaporin-2 pathway: recent advances in understanding water balance disorders.F1000Research · 2019Review
- CONGENITAL NEPHROGENIC DIABETES INSIPIDUS IN A PRETERM INFANT: CASE PRESENTATION.Acta endocrinologica (Bucharest, Romania : 2005)Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Congenital nephrogenic diabetes insipidus (NDI) is characterized by defective urine concentrating ability. Symptomatic polyuria is present from birth, even with normal release of the antidiuretic hormone vasopressin by the pituitary. Over the last two decades, the aquaporin-2 (AQP2) gene has been cloned and the molecular mechanisms of urine concentration have been gradually elucidated. Vasopressin binds to the vasopressin type II receptor (V2R) in the renal collecting ducts and then activates AQP2 phosphorylation and trafficking to increase water reabsorption from urine. Most cases of congenital NDI are caused by loss-of-function mutations to V2R, resulting in unresponsiveness to vasopressin. In this article, we provide an overview of novel therapeutic molecules of congenital NDI that can activate AQP2 by bypassing defective V2R signaling with a particular focus on the activators of the calcium and cAMP signaling pathways.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.