ReviewAmerican journal of physiology. Renal physiology2013
Novel role of ouabain as a cystogenic factor in autosomal dominant polycystic kidney disease.
Review in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 29 citations in OpenAlex.
- The pathophysiological significance between autosomal dominant polycystic kidney disease and neutrophil gelatinase-associated lipocalin.Kidney research and clinical practice · 2025Article
- Arterial Hypertension: Novel Pharmacological Targets and Future Perspectives.Journal of clinical medicine · 2024Review
- Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024Review
- Ouabain enhances renal cyst growth in a slowly progressive mouse model of autosomal dominant polycystic kidney disease.American journal of physiology. Renal physiology · 2023Article
- A NaFrontiers in cell and developmental biology · 2021Article
- Prostaglandin E2 stimulates the epithelial sodium channel (ENaC) in cultured mouse cortical collecting duct cells in an autocrine manner.The Journal of general physiology · 2020Article
- A caveolin binding motif in Na/K-ATPase is required for stem cell differentiation and organogenesis in mammals andScience advances · 2020Article
- 21-Benzylidene digoxin decreases proliferation by inhibiting the EGFR/ERK signaling pathway and induces apoptosis in HeLa cells.Steroids · 2020Article
- Novel Medical Treatments for Hypertension and Related Comorbidities.Current hypertension reports · 2018Review
- Na/K-ATPase Y260 Phosphorylation-mediated Src Regulation in Control of Aerobic Glycolysis and Tumor Growth.Scientific reports · 2018Article
- Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal Diseases.International journal of molecular sciences · 2018Review
- Ouabain-induced apoptosis and inhibition of viability of tubulointerstitial cells by regulating NKA/pSrc/pERK/pAkt/pS6k/caspase 3 may contribute to lupus nephritis development.International journal of clinical and experimental pathology · 2018Article
- Ouabain promotes partial epithelial to mesenchymal transition (EMT) changes in human autosomal dominant polycystic kidney disease (ADPKD) cells.Experimental cell research · 2017Article
- Protein Interaction and Na/K-ATPase-Mediated Signal Transduction.Molecules (Basel, Switzerland) · 2017Review
- On the Many Actions of Ouabain: Pro-Cystogenic Effects in Autosomal Dominant Polycystic Kidney Disease.Molecules (Basel, Switzerland) · 2017Review
- Much More than a Cardiotonic Steroid: Modulation of Inflammation by Ouabain.Frontiers in physiology · 2017Review
- Ouabain Enhances ADPKD Cell Apoptosis via the Intrinsic Pathway.Frontiers in physiology · 2016Article
- Ouabain Regulates CFTR-Mediated Anion Secretion and Na,K-ATPase Transport in ADPKD Cells.The Journal of membrane biology · 2015Article
- Urinary biomarkers at early ADPKD disease stage.PloS one · 2015Article
- Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The classic role of the Na-K-ATPase is that of a primary active transporter that utilizes cell energy to establish and maintain transmembrane Na(+) and K(+) gradients to preserve cell osmotic stability, support cell excitability, and drive secondary active transport. Recent studies have revealed that Na-K-ATPase located within cholesterol-containing lipid rafts serves as a receptor for cardiotonic steroids, including ouabain. Traditionally, ouabain was viewed as a toxin produced only in plants, and it was used in relatively high concentrations to experimentally block the pumping action of the Na-K-ATPase. However, the new and unexpected role of the Na-K-ATPase as a signal transducer revealed a novel facet for ouabain in the regulation of a myriad of cell functions, including cell proliferation, hypertrophy, apoptosis, mobility, and metabolism. The seminal discovery that ouabain is endogenously produced in mammals and circulates in plasma has fueled the interest in this endogenous molecule as a potentially important hormone in normal physiology and disease. In this article, we review the role of the Na-K-ATPase as an ion transporter in the kidney, the experimental evidence for ouabain as a circulating hormone, the function of the Na-K-ATPase as a signal transducer that mediates ouabain's effects, and novel results for ouabain-induced Na-K-ATPase signaling in cystogenesis of autosomal dominant polycystic kidney disease.
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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.