ArticleClinical and translational science2009
Targeted disruption of K(ATP) channels aggravates cardiac toxicity in cocaine abuse.
Article in Clinical and translational science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 11 citations in OpenAlex.
- Stimulant Drugs of Abuse and Cardiac Arrhythmias.Circulation. Arrhythmia and electrophysiology · 2022Review
- Cocaine Hydrolase Gene Transfer Demonstrates Cardiac Safety and Efficacy against Cocaine-Induced QT Prolongation in Mice.The Journal of pharmacology and experimental therapeutics · 2016Article
- Nicotinamide-rich diet improves physical endurance by up-regulating SUR2A in the heart.Journal of cellular and molecular medicine · 2011Article
- Advances in cardiac ATP-sensitive K+ channelopathies from molecules to populations.Circulation. Arrhythmia and electrophysiology · 2011Article
- K(ATP) channels process nucleotide signals in muscle thermogenic response.Critical reviews in biochemistry and molecular biology · 2010Article
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 at 2 institutions in 1 country.
Funding
Abstract
Cocaine is the most frequently used illicit drug among individuals seeking emergency-room care, with fatal outcome most often attributable to the cardiovascular manifestations of drug abuse. While the symptomatic presentations of cocaine toxicity are increasingly understood, the molecular determinants that define outcome remain largely unknown. Here, we report that the susceptibility to cocaine-induced cardiotoxicity is genetically regulated. Targeted deletion of the KCNJ11-encoded Kir6.2 pore-forming subunit of sarcolemmal K(ATP) channels resulted in amplified vulnerability to the toxic effects of chronic cocaine abuse. Under the hyperadrenergic stress, imposed by daily 3-week-long intraperitoneal administration of 30 mg/kg cocaine in Kir6.2-knockout mice, failure to maintain cardiac homeostasis translated into decreased exercise tolerance revealed by poor treadmill stress performance, and dilated hypokinetic left hearts with aggravated cellular hypertrophy and pathognomonic characteristics of chronic cocaine-induced cardiac toxicity. This study therefore reveals a previously unrecognized role of Kir6.2-encoded K(ATP) channels in determining cardiovascular outcome in chronic cocaine abuse, identifying a novel molecular determinant of cocaine cardiotoxicity.
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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.