ArticleThe Journal of clinical investigation2011
Oxidized CaMKII: a "heart stopper" for the sinus node?
Article in The Journal of clinical investigation, 2011. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Insulin sensitization causes accelerated sinus nodal dysfunction through autophagic dysregulation in hypertensive mice.Translational and clinical pharmacology · 2021Article
- Molecular and tissue mechanisms of catecholaminergic polymorphic ventricular tachycardia.The Journal of physiology · 2020Review
- Targeting CaFrontiers in physiology · 2020Review
- Mitochondrial-Mediated Oxidative CaJournal of the American Heart Association · 2018Article
- Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes Mellitus.Frontiers in physiology · 2018Review
- Function and dysfunction of human sinoatrial node.Korean circulation journal · 2015Review
- Sinus node dysfunction in catecholaminergic polymorphic ventricular tachycardia: risk factor and potential therapeutic target?Trends in cardiovascular medicine · 2014Review
- CaMKII in sinoatrial node physiology and dysfunction.Frontiers in pharmacology · 2014Review
Corrections and comments
- Comment on
Authors and funding
2 authors.
Funding
Abstract
Each normal heart beat is triggered by an electrical impulse emitted from a group of specialized cardiomyocytes that together form the sinoatrial node (SAN). In this issue of the JCI, Swaminathan and colleagues demonstrate a new molecular mechanism that can disrupt the normal beating of the heart: angiotensin II - typically found in increased levels in heart failure and hypertension - oxidizes and activates Ca2+/calmodulin-dependent kinase II via NADPH oxidase activation, causing SAN cell death. The loss of SAN cells produces an electrical imbalance termed the "source-sink mismatch," which may contribute to the SAN dysfunction that affects millions of people later in life and complicates a number of heart diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.