ReviewNature reviews. Nephrology2015
Vasopressin and disruption of calcium signalling in polycystic kidney disease.
Review in Nature reviews. Nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
77 citing papers in PubMed, 136 citations in OpenAlex.
- Review
- Characterization of Kidney and Liver Cystic Phenotype Associated with GANAB Using Advanced Imaging Biomarkers.Nephron · 2026Article
- Contemporary management of advanced chronic kidney disease: An evidence-based review.European journal of internal medicine · 2026Review
- Autosomal dominant polycystic kidney disease: an overview of recent genetic and clinical advances.Renal failure · 2025Review
- Cleavage of N-terminus of polycystin-1 increases calcium permeability of polycystin-1/2 receptor channel complexes.JCI insight · 2025Article
- Prostaglandin Analogs and Eupatilin as Treatments for Nephronophthisis.Kidney international reports · 2025Article
- Targeting GLP-1 Signaling Ameliorates Cystogenesis in a Zebrafish Model of Nephronophthisis.International journal of molecular sciences · 2025Article
- Kidney organoid models of polycystic kidney disease: challenges and future directions.American journal of physiology. Renal physiology · 2025Review
- Cilia at the crossroad: convergence of regulatory mechanisms to govern cilia dynamics during cell signaling and the cell cycle.Cell & bioscience · 2025Review
- Advanced Strategies in Enhancing the Hepatoprotective Efficacy of Natural Products: Integrating Nanotechnology, Genomics, and Mechanistic Insights.ACS biomaterials science & engineering · 2025Review
- Methods to Assess Neuronal Primary Cilia Electrochemical Signaling.Journal of cellular physiology · 2025Article
- PKD1 mutation perturbs morphogenesis in tubular epithelial organoids derived from human pluripotent stem cells.Scientific reports · 2025Article
- Tolvaptan safety in autosomal-dominant polycystic kidney disease; a focus on idiosyncratic drug-induced liver injury liabilities.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
- Calcium signalling and transport in the kidney.Nature reviews. Nephrology · 2024Review
- Spontaneous Coronary Artery Dissection in Patients with Autosomal Dominant Polycystic Kidney Disease: A Systematic Review of the Literature.Journal of personalized medicine · 2024Review
- Mechanistic complement of autosomal dominant polycystic kidney disease: the role of aquaporins.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Neuroimmune interplay in kidney health and disease: Role of renal nerves.Autonomic neuroscience : basic & clinical · 2023Review
- Prioritized polycystic kidney disease drug targets and repurposing candidates from pre-cystic and cystic mouse Pkd2 model gene expression reversion.Molecular medicine (Cambridge, Mass.) · 2023Article
- Recent updates in therapeutic approach using tolvaptan for autosomal dominant polycystic kidney disease.The Korean journal of internal medicine · 2023Review
- Metabolism-based approaches for autosomal dominant polycystic kidney disease.Frontiers in molecular biosciences · 2023Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic kidney disease and is responsible for 5-10% of cases of end-stage renal disease worldwide. ADPKD is characterized by the relentless development and growth of cysts, which cause progressive kidney enlargement associated with hypertension, pain, reduced quality of life and eventual kidney failure. Mutations in the PKD1 or PKD2 genes, which encode polycystin-1 (PC1) and polycystin-2 (PC2), respectively, cause ADPKD. However, neither the functions of these proteins nor the molecular mechanisms of ADPKD pathogenesis are well understood. Here, we review the literature that examines how reduced levels of functional PC1 or PC2 at the primary cilia and/or the endoplasmic reticulum directly disrupts intracellular calcium signalling and indirectly disrupts calcium-regulated cAMP and purinergic signalling. We propose a hypothetical model in which dysregulated metabolism of cAMP and purinergic signalling increases the sensitivity of principal cells in collecting ducts and of tubular epithelial cells in the distal nephron to the constant tonic action of vasopressin. The resulting magnified response to vasopressin further enhances the disruption of calcium signalling that is initiated by mutations in PC1 or PC2, and activates downstream signalling pathways that cause impaired tubulogenesis, increased cell proliferation, increased fluid secretion and interstitial inflammation.
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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.