ArticlePflugers Archiv : European journal of physiology2024
The mechanism of 25-hydroxycholesterol-mediated suppression of atrial β1-adrenergic responses.
Article in Pflugers Archiv : European journal of physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 6 citations in OpenAlex.
- Age-related changes in adrenergic regulation of contractility and redox status of glycolytic and oxidative skeletal muscles.GeroScience · 2026Article
- The beta1-adrenergic receptor in the heart.Cell death discovery · 2025Review
- Increased 25-hydroxycholesterol as an indicator for patients with vestibular neuritis.Frontiers in neurology · 2025Article
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
25-Hydroxycholesterol (25HC) is a biologically active oxysterol, whose production greatly increases during inflammation by macrophages and dendritic cells. The inflammatory reactions are frequently accompanied by changes in heart regulation, such as blunting of the cardiac β-adrenergic receptor (AR) signaling. Here, the mechanism of 25HC-dependent modulation of responses to β-AR activation was studied in the atria of mice. 25HC at the submicromolar levels decreased the β-AR-mediated positive inotropic effect and enhancement of the Ca
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