ReviewHeart rhythm2010
Ion channel trafficking: a new therapeutic horizon for atrial fibrillation.
Review in Heart rhythm, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 23 citations in OpenAlex.
- Gene modules and genes associated with postoperative atrial fibrillation: weighted gene co-expression network analysis and circRNA-miRNA-mRNA regulatory network analysis.Journal of thoracic disease · 2023Article
- Small-conductance calcium-activated potassium channels in the heart: expression, regulation and pathological implications.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Modulation of IJournal of cellular physiology · 2022Article
- KInternational journal of molecular sciences · 2021Article
- Small Conductance CaFrontiers in physiology · 2021Article
- Altering integrin engagement regulates membrane localization of KJournal of cell science · 2019Article
- Polycomb-dependent repression of the potassium channel-encoding gene KCNA5 promotes cancer cell survival under conditions of stress.Oncogene · 2015Article
- Functional interaction with filamin A and intracellular Ca2+ enhance the surface membrane expression of a small-conductance Ca2+-activated K+ (SK2) channel.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Improved functional expression of human cardiac kv1.5 channels and trafficking-defective mutants by low temperature treatment.PloS one · 2014Article
- Shear stress triggers insertion of voltage-gated potassium channels from intracellular compartments in atrial myocytes.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Trafficking of intermediate (KCa3.1) and small (KCa2.x) conductance, Ca(2+)-activated K(+) channels: a novel target for medicinal chemistry efforts?ChemMedChem · 2012Review
- Novel molecular targets for atrial fibrillation therapy.Nature reviews. Drug discovery · 2012Review
- The Na+/K+ pump is an important modulator of refractoriness and rotor dynamics in human atrial tissue.American journal of physiology. Heart and circulatory physiology · 2012Article
- ESCRT-dependent targeting of plasma membrane localized KCa3.1 to the lysosomes.American journal of physiology. Cell physiology · 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Atrial fibrillation (AF) is a common cardiac arrhythmia with potentially life-threatening complications. Drug therapies for treatment of AF that seek long-term maintenance of normal sinus rhythm remain elusive due in large part to proarrhythmic ventricular actions. Kv1.5, which underlies the atrial specific I(Kur) current, is a major focus of research efforts seeking new therapeutic strategies and targets. Recent work has shown a novel effect of antiarrhythmic drugs where compounds that block Kv1.5 channel current also can alter ion channel trafficking. This work further suggests that the pleiotropic effects of antiarrhythmic drugs may be separable. Although this finding highlights the therapeutic potential for selective manipulation of ion channel surface density, it also reveals an uncertainty regarding the specificity of modulating trafficking pathways without risk of off-target effects. Future studies may show that specific alteration of Kv1.5 trafficking can overcome the proarrhythmic limitations of current pharmacotherapy and provide an effective method for long-term cardioversion in AF.
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.