ArticleJACC. Clinical electrophysiology2025
Effect of the Membrane Environment on Pharmacologic Inhibition of hERG K
Article in JACC. Clinical electrophysiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Lipid-dependent regulation of Kv10.1 in cancer: implications of membrane remodeling for channel function and pharmacology.Frontiers in pharmacology · 2026Review
- Roles of funny HCN.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundhERG encodes K
objectivesBecause hERG channels reside in cholesterol rich lipid raft domains, we hypothesized that disrupting the membrane environment by depleting cholesterol might alter inhibition of channel activity by certain drugs.
methodsWe tested our hypothesis by examining the effect that depleting membrane cholesterol with methyl-β-cyclodextrin has on the ability of several compounds to inhibit hERG channels expressed in HEK293 cells.
resultsWe found that cholesterol depletion significantly increased the sensitivity of the whole cell current to inhibition by ibutilide, while decreasing the currents sensitivity to dofetilide and amiodarone at negative membrane potentials.
conclusionsThese results support the idea that the lipid environment of the plasma membrane plays a role in the ability of certain drugs to inhibit hERG channel activity. Differences in membrane cholesterol content may affect the ability of some hERG channel blockers to produce arrhythmogenic behavior.
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