ReviewBiochimica et biophysica acta2010
The sodium pump and cardiotonic steroids-induced signal transduction protein kinases and calcium-signaling microdomain in regulation of transporter trafficking.
Review in Biochimica et biophysica acta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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
74 citing papers in PubMed, 120 citations in OpenAlex.
- CMolecules (Basel, Switzerland) · 2026Article
- Laminaran Attenuates NaCl-Induced Cytotoxicity via ROS Scavenging and Prevents Alteration of Cellular Elastic Modulus.Marine drugs · 2026Article
- Na/K-ATPase in the renal proximal tubule cell: classic & novel roles in sodium handling.Frontiers in physiology · 2026Review
- Bufalin-Induced Epithelial-to-Mesenchymal Transition in Kidney Epithelial Cells.Cell biology international · 2025Article
- Beta-amyloid influences the content and trafficking of beta-amyloid precursor protein via Na,K-ATPase-Src kinase positive feedback loop.Frontiers in pharmacology · 2025Article
- Factors that influence the Na/K-ATPase signaling and function.Frontiers in pharmacology · 2025Review
- Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024Review
- Involvement of the NaInternational journal of molecular sciences · 2024Article
- The vascular Na,K-ATPase: clinical implications in stroke, migraine, and hypertension.Clinical science (London, England : 1979) · 2023Review
- New Insights on the Role of Marinobufagenin from Bench to Bedside in Cardiovascular and Kidney Diseases.International journal of molecular sciences · 2023Review
- Timed use of digoxin prevents heart ischemia-reperfusion injury through a REV-ERBα-UPS signaling pathway.Nature cardiovascular research · 2022Article
- Neuroinflammation and Neutrophils: Modulation by Ouabain.Frontiers in pharmacology · 2022Review
- Na,K-ATPase as a target for endogenous cardiotonic steroids: What's the evidence?Genes & diseases · 2021Review
- Cardiac Oxidative Signaling and Physiological Hypertrophy in the Na/K-ATPase α1International journal of molecular sciences · 2021Article
- Predicting Nonalcoholic Fatty Liver Disease through a Panel of Plasma Biomarkers and MicroRNAs in Female West Virginia Population.International journal of molecular sciences · 2020Article
- The αScientific reports · 2020Article
- Elucidating Potential Profibrotic Mechanisms of Emerging Biomarkers for Early Prognosis of Hepatic Fibrosis.International journal of molecular sciences · 2020Review
- The Na/K-ATPase α1 and c-Src form signaling complex under native condition: A crosslinking approach.Scientific reports · 2020Article
- Ouabain-Induced Cell Death and Survival. Role of α1-Na,K-ATPase-Mediated Signaling and [NaFrontiers in physiology · 2020Review
- Cardiotonic Steroids-A Possible Link Between High-Salt Diet and Organ Damage.International journal of molecular sciences · 2019Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The Na/K-ATPase was discovered as an energy transducing ion pump. A major difference between the Na/K-ATPase and other P-type ATPases is its ability to bind a group of chemicals called cardiotonic steroids (CTS). The plant-derived CTS such as digoxin are valuable drugs for the management of cardiac diseases, whereas ouabain and marinobufagenin (MBG) have been identified as a new class of endogenous hormones. Recent studies have demonstrated that the endogenous CTS are important regulators of renal Na(+) excretion and blood pressure. The Na/K-ATPase is not only an ion pump, but also an important receptor that can transduce the ligand-like effect of CTS on intracellular protein kinases and Ca(2+) signaling. Significantly, these CTS-provoked signaling events are capable of reducing the surface expression of apical NHE3 (Na/H exchanger isoform 3) and basolateral Na/K-ATPase in renal proximal tubular cells. These findings suggest that endogenous CTS may play an important role in regulation of tubular Na(+) excretion under physiological conditions; conversely, a defect at either the receptor level (Na/K-ATPase) or receptor-effector coupling would reduce the ability of renal proximal tubular cells to excrete Na(+), thus culminating/resulting in salt-sensitive hypertension.
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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.