ArticleBritish journal of pharmacology2019
Trichostatin A blocks aldosterone-induced Na
Article in British journal of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 12 citations in OpenAlex.
- Genetic and Epigenetic Mechanisms Regulating Blood Pressure and Kidney Dysfunction.Hypertension (Dallas, Tex. : 1979) · 2024Review
- Histone Modifications and Their Contributions to Hypertension.Hypertension (Dallas, Tex. : 1979) · 2024Review
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021Article
- Posttranslational Modifications of the Mineralocorticoid Receptor and Cardiovascular Aging.Frontiers in molecular biosciences · 2021Review
- 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
- Histone Deacetylases in Kidney Physiology and Acute Kidney Injury.Seminars in nephrology · 2020Review
- Trichostatin A blocks aldosterone-induced NaBritish journal of pharmacology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeAldosterone stimulates epithelial Na EXPERIMENTAL APPROACH: Electrometric and molecular methods were used to define the effects of a pan-KDAC inhibitor, trichostatin A, on the responses to a physiologically relevant concentration of aldosterone (3 nM) in murine mCCD KEY
resultsAldosterone augmented ENaC-induced Na CONCLUSIONS AND IMPLICATIONS: Inhibition of lysine de-acetylation suppresses aldosterone-dependent control over the SGK1-ENaC pathway but does not perturb post-transcriptional signalling, providing a physiological basis for the anti-hypertensive action of KDAC inhibition seen in vivo.
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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.