ReviewJournal of cellular physiology2019
Autosomal dominant polycystic kidney disease: Disrupted pathways and potential therapeutic interventions.
Review in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Exploring multiple drug actions of a CaNaunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Unravelling sex-specific differences in autosomal dominant polycystic kidney disease: a multiorgan perspective.Clinical kidney journal · 2026Review
- Genomic and epigenomic landscape of ADPKD: towards precision diagnostics and tailored treatments.Frontiers in epigenetics and epigenomics · 2026Review
- Review
- Metabolic Reprogramming in Autosomal Dominant Polycystic Kidney Disease: Role in Cystogenesis and Novel Therapeutic Approaches.Biomedicines · 2025Review
- Review
- Calcium signaling in polycystic kidney disease- cell death and survival.Cell calcium · 2023Review
- Overexpression of notch signaling in renin cells leads to a polycystic kidney phenotype.Clinical science (London, England : 1979) · 2023Article
- Polycystin-1 Is a Crucial Regulator of BIN1 Expression and T-Tubule Remodeling Associated with the Development of Dilated Cardiomyopathy.International journal of molecular sciences · 2022Article
- Organoid-on-a-chip model of human ARPKD reveals mechanosensing pathomechanisms for drug discovery.Science advances · 2022Article
- Identification of novel single-nucleotide variants altering RNA splicing of PKD1 and PKD2.Journal of human genetics · 2022Article
- Involvement of ceramide biosynthesis in increased extracellular vesicle release inFrontiers in endocrinology · 2022Article
- The tyrosine-kinase inhibitor Nintedanib ameliorates autosomal-dominant polycystic kidney disease.Cell death & disease · 2021Article
- MRTF: Basic Biology and Role in Kidney Disease.International journal of molecular sciences · 2021Review
- Combination of curcumin and ginkgolide B inhibits cystogenesis by regulating multiple signaling pathways.Molecular medicine reports · 2021Article
- Retarding Progression of Chronic Kidney Disease in Autosomal Dominant Polycystic Kidney Disease with Metformin and Other Therapies: An Update of New Insights.International journal of general medicine · 2021Review
- Insights Into the Molecular Mechanisms of Polycystic Kidney Diseases.Frontiers in physiology · 2021Review
- Targeting E3 Ubiquitin Ligases and Deubiquitinases in Ciliopathy and Cancer.International journal of molecular sciences · 2020Review
- Ciliary Genes in Renal Cystic Diseases.Cells · 2020Review
- SNX9 Inhibits Cell Proliferation and Cyst Development in Autosomal Dominant Polycystic Kidney Disease via Activation of the Hippo-YAP Signaling Pathway.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is a monogenic inherited renal cystic disease that occurs in different races worldwide. It is characterized by the development of a multitude of renal cysts, which leads to massive enlargement of the kidney and often to renal failure in adulthood. ADPKD is caused by a mutation in PKD1 or PKD2 genes encoding the proteins polycystin-1 and polycystin-2, respectively. Recent studies showed that cyst formation and growth result from deregulation of multiple cellular pathways like proliferation, apoptosis, metabolic processes, cell polarity, and immune defense. In ADPKD, intracellular cyclic adenosine monophosphate (cAMP) promotes cyst enlargement by stimulating cell proliferation and transepithelial fluid secretion. Several interventions affecting many of these defective signaling pathways have been effective in animal models and some are currently being tested in clinical trials. Moreover, the stem cell therapy can improve nephropathies and according to studies were done in this field, can be considered as a hopeful therapeutic approach in future for PKD. This study provides an in-depth review of the relevant molecular pathways associated with the pathogenesis of ADPKD and their implications in development of potential therapeutic strategies.
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Registered trials
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.