ReviewInternational journal of molecular sciences2018
Na⁺, K⁺-ATPase Signaling and Bipolar Disorder.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 63 citations in OpenAlex.
- Astrocyte redox imbalance underlies prelimbic neuronal hypoactivity and maladaptive affective behaviors in epilepsy.Science advances · 2026Article
- Thyroid hormone augmentation for bipolar disorder: a neurobiological and clinical narrative review.International journal of bipolar disorders · 2026Review
- Functional implications of polygenic risk for schizophrenia in human neurons.Nature communications · 2026Article
- Glucagon-like Peptide-1 receptor agonists as emerging therapeutics in bipolar disorder: a narrative review of preclinical and clinical evidence.Molecular psychiatry · 2026Review
- Light-based 40 Hz sensory therapy for brain disorders: physiological basis, therapeutic mechanisms, and future prospects.Frontiers in medicine · 2026Review
- Effects of chronic nicotine administration on behavioral parameters and Na⁺/K⁺-ATPase mRNA expression in the brains of male Swiss Albino mice exposed to chronic stress during adolescence.BMC pharmacology & toxicology · 2025Article
- Unveiling the role of Na⁺/K⁺-ATPase pump: neurodegenerative mechanisms and therapeutic horizons.Pharmacological reports : PR · 2025Review
- Na,K-ATPase mediated and cardiotonic induced signaling in health and disease.Frontiers in physiology · 2025Review
- Involvement of the NaInternational journal of molecular sciences · 2024Article
- The Oxidative Status and NaBioMed research international · 2024Article
- Chronic Ouabain Targets Pore-Forming Claudin-2 and Ameliorates Radiation-Induced Damage to the Rat Intestinal Tissue Barrier.International journal of molecular sciences · 2023Article
- Short-Term Mild Hypoxia Modulates Na,K-ATPase to Maintain Membrane Electrogenesis in Rat Skeletal Muscle.International journal of molecular sciences · 2022Article
- Chronic Ouabain Prevents Radiation-Induced Reduction in the α2 Na,K-ATPase Function in the Rat Diaphragm Muscle.International journal of molecular sciences · 2022Article
- RETRACTED: Activating SIRT-1 Signalling with the Mitochondrial-CoQ10 Activator Solanesol Improves Neurobehavioral and Neurochemical Defects in Ouabain-Induced Experimental Model of Bipolar Disorder.Pharmaceuticals (Basel, Switzerland) · 2022Article
- NMDA receptor inhibition prevents intracellular sodium elevations in human olfactory neuroepithelial precursors derived from bipolar patients.Scientific reports · 2022Article
- Imipramine induces hyperactivity in rats pretreated with ouabain: Implications to the mania switch induced by antidepressants.Journal of affective disorders · 2022Article
- Endogenous Cardiac Steroids in Bipolar Disorder: State of the Art.International journal of molecular sciences · 2022Review
- Oleandrin: A Systematic Review of its Natural Sources, Structural Properties, Detection Methods, Pharmacokinetics and Toxicology.Frontiers in pharmacology · 2022Review
- Bipolar spectrum disorders in neurologic disorders.Frontiers in psychiatry · 2022Review
- Regulatory effect of insulin on the structure, function and metabolism of NaExperimental and therapeutic medicine · 2021Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bipolar disorder (BD) is a severe and common chronic mental illness characterized by recurrent mood swings between depression and mania. The biological basis of the disease is poorly understood and its treatment is unsatisfactory. Although in past decades the "monoamine hypothesis" has dominated our understanding of both the pathophysiology of depressive disorders and the action of pharmacological treatments, recent studies focus on the involvement of additional neurotransmitters/neuromodulators systems and cellular processes in BD. Here, evidence for the participation of Na⁺, K⁺-ATPase and its endogenous regulators, the endogenous cardiac steroids (ECS), in the etiology of BD is reviewed. Proof for the involvement of brain Na⁺, K⁺-ATPase and ECS in behavior is summarized and it is hypothesized that ECS-Na⁺, K⁺-ATPase-induced activation of intracellular signaling participates in the mechanisms underlying BD. We propose that the activation of ERK, AKT, and NFκB, resulting from ECS-Na⁺, K⁺-ATPase interaction, modifies neuronal activity and neurotransmission which, in turn, participate in the regulation of behavior and BD. These observations suggest Na⁺, K⁺-ATPase-mediated signaling is a potential target for drug development for the treatment of BD.
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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.