ArticleCardiovascular research2014
Cardiac hypertrophy in mice expressing unphosphorylatable phospholemman.
Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 42 citations in OpenAlex.
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- Temporal changes in first-phase ejection fraction during evolution of heart failure with preserved ejection fraction and afterload-induced heart failure in mice.Journal of physiology and biochemistry · 2026Article
- FXYD1 was identified as a hub gene in recurrent miscarriage and involved in decidualization via regulating Na/K-ATPase activity.Journal of assisted reproduction and genetics · 2025Article
- Role of NaInternational journal of molecular sciences · 2024Review
- The Na/K-ATPase α1/Src Signaling Axis Regulates Mitochondrial Metabolic Function and Redox Signaling in Human iPSC-Derived Cardiomyocytes.Biomedicines · 2023Article
- Changes in cellular CaThe Journal of physiology · 2023Article
- Non-Selective PDE4 Inhibition Induces a Rapid and Transient Decrease of Serum Potassium in Mice.Biology · 2022Article
- Dynamic but discordant alterations in zDHHC5 expression and palmitoylation of its substrates in cardiac pathologies.Frontiers in physiology · 2022Article
- FXYD proteins and sodium pump regulatory mechanisms.The Journal of general physiology · 2021Review
- Phospholemman Phosphorylation Regulates Vascular Tone, Blood Pressure, and Hypertension in Mice and Humans.Circulation · 2021Article
- Intracellular sodium elevation reprograms cardiac metabolism.Nature communications · 2020Article
- Endogenous cardiotonic steroids and cardiovascular disease, where to next?Cell calcium · 2020Review
- Paternal Resistance Training Induced Modifications in the Left Ventricle Proteome Independent of Offspring Diet.Oxidative medicine and cellular longevity · 2020Article
- p38γ MAPK contributes to left ventricular remodeling after pathologic stress and disinhibits calpain through phosphorylation of calpastatin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Increased myocardial sodium signal intensity in Conn's syndrome detected by 23Na magnetic resonance imaging.European heart journal. Cardiovascular Imaging · 2019Article
- Heart failure leads to altered β2-adrenoceptor/cyclic adenosine monophosphate dynamics in the sarcolemmal phospholemman/Na,K ATPase microdomain.Cardiovascular research · 2019Article
- Is there a causal link between intracellular Na elevation and metabolic remodelling in cardiac hypertrophy?Biochemical Society transactions · 2018Review
- The Role of Sodium in Diabetic Cardiomyopathy.Frontiers in physiology · 2018Review
- Hypokalemia-Induced Arrhythmias and Heart Failure: New Insights and Implications for Therapy.Frontiers in physiology · 2018Review
- Myocyte [NaFrontiers in physiology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
aimsElevation of intracellular Na in the failing myocardium contributes to contractile dysfunction, the negative force-frequency relationship, and arrhythmias. Although phospholemman (PLM) is recognized to form the link between signalling pathways and Na/K pump activity, the possibility that defects in its regulation contribute to elevation of intracellular Na has not been investigated. Our aim was to test the hypothesis that the prevention of PLM phosphorylation in a PLM(3SA) knock-in mouse (in which PLM has been rendered unphosphorylatable) will exacerbate cardiac hypertrophy and cellular Na overload. Testing this hypothesis should determine whether changes in PLM phosphorylation are simply bystander effects or are causally involved in disease progression. METHODS AND
resultsIn wild-type (WT) mice, aortic constriction resulted in hypophosphorylation of PLM with no change in Na/K pump expression. This under-phosphorylation of PLM occurred at 3 days post-banding and was associated with a progressive decline in Na/K pump current and elevation of [Na]i. Echocardiography, morphometry, and pressure-volume (PV) catheterization confirmed remodelling, dilation, and contractile dysfunction, respectively. In PLM(3SA) mice, expression of Na/K ATPase was increased and PLM decreased such that net Na/K pump current under quiescent conditions was unchanged (cf. WT myocytes); [Na(+)]i was increased and forward-mode Na/Ca exchanger was reduced in paced PLM(3SA) myocytes. Cardiac hypertrophy and Na/K pump inhibition were significantly exacerbated in banded PLM(3SA) mice compared with banded WT.
conclusionsDecreased phosphorylation of PLM reduces Na/K pump activity and exacerbates Na overload, contractile dysfunction, and adverse remodelling following aortic constriction in mice. This suggests a novel therapeutic target for the treatment of heart failure.
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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.