ArticleTransactions of the American Clinical and Climatological Association2008
Delivery of ion channel genes to treat cardiovascular diseases.
Article in Transactions of the American Clinical and Climatological Association, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- MicroRNA expression signatures of atrial fibrillation: The critical systematic review and bioinformatics analysis.Experimental biology and medicine (Maywood, N.J.) · 2020Pooled it
- Ion channel remodeling in vascular smooth muscle during hypertension: Implications for novel therapeutic approaches.Pharmacological research · 2013Review
- Ca(V)1.2 channel N-terminal splice variants modulate functional surface expression in resistance size artery smooth muscle cells.The Journal of biological chemistry · 2011Article
- The ß subunit of voltage-gated Ca2+ channels.Physiological reviews · 2010Review
- Smooth muscle cell alpha2delta-1 subunits are essential for vasoregulation by CaV1.2 channels.Circulation research · 2009Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Modifying ion channel expression and function in the heart and vasculature are potentially useful, novel approaches to managing cardiac hypertrophy, atrial fibrillation and hypertension. Calcium channels play a pivotal role in the heart and vasculature in controlling muscle contraction as well as other aspects of calcium-dependent signaling. The present investigation reports development of mutated L-type calcium channel beta subunits that are delivered by an adenoviral vector to vascular smooth muscle tissue. Wild type subunits serve a chaperone function for the pore-forming alpha(1C) subunit of the calcium channel, localize to the cell membrane and enhance calcium current. Conversely, mutated subunits function as dominant negative, defective chaperone molecules that disrupt targeting to the cell membrane and decrease calcium current. The dominant negative genes can be delivered in vitro and ex vivo, and have the potential to decrease arterial tone and lower blood pressure in vivo.
Indexed as
Identifiers
18596857PMC2394695W106668870What 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.