Evidence map›Paper›PMID 28642118›Full record

ReviewPharmacology & therapeutics2017

Current state of the art for cardiac arrhythmia gene therapy.

J Kevin Donahue

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 23% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Gene therapy for atrial fibrillation.Journal of molecular and cellular cardiology · 2024
    Review
  2. Review
  3. Article
  4. Article
  5. Recent advances in gene therapy for atrial fibrillation.Journal of cardiovascular electrophysiology · 2021
    Review
  6. Review
  7. Big Data and Atrial Fibrillation: Current Understanding and New Opportunities.Journal of cardiovascular translational research · 2020
    Review
  8. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

J Kevin DonahueUniversity of Massachusetts Medical School, Division of Cardiology, 55 Lake Ave. North, Worcester, MA 01655, United States. Electronic address: kevin.donahue@umassmed.edu.
University of Massachusetts Chan Medical School · US

Funding

Final preclinical development of AAV gene therapy for atrial fibrillationR01HL130376 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DONAHUE, J KEVIN · 2016 to 2019
$2.9M
Integrative analysis of electrophysiology in the healed myocardial infarction scarR01HL134185 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DONAHUE, J KEVIN · 2017 to 2020
$2.8M
GENE TRANSFER APPROACHES TO ATRIAL FIBRILATIONR01HL093486 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DONAHUE, J KEVIN · 2008 to 2012
$2.0M
Preclinical gene therapy development for post-operative atrial fibrillationR21AG042701 · NIA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DONAHUE, J KEVIN · 2013 to 2014
$442k
NHLBI NIH HHS R01 HL093486NHLBI NIH HHS R01 HL130376NHLBI NIH HHS R01 HL134185NIA NIH HHS R21 AG042701
6 · The paper itself

Abstract

Cardiac arrhythmias are a leading cause of morbidity and mortality. Currently available therapeutic options lack sufficient efficacy and safety. Gene therapy has been proposed for treatment of cardiac arrhythmias. This review will discuss the current state of development for arrhythmia gene therapy. So far, all published studies are short-term, proof-of-concept animal studies. Potential replacement of cardiac pacemakers has been shown for combination gene therapy using the HCN2 gene and either the gene for adenylate cyclase, the skeletal muscle isoform of the sodium channel, or a dominant negative mutant of the potassium channel responsible for resting membrane potential. Atrial fibrillation has been prevented by gene transfer of either a dominant negative mutant of a repolarizing potassium channel, a gap junction, or an siRNA directed against caspase 3. Inherited arrhythmia syndromes have been corrected by replacement of the causative genes. Post-infarct ventricular tachycardia has been reduced by gene therapy with the skeletal muscle sodium channel and connexins and eliminated with the dominant negative mutant of the potassium channel responsible for resting membrane potential. These ideas show considerable promise. Long-term efficacy and safety studies are required to see if they can become viable therapies.

Indexed as

Genetic TherapyAnimalsArrhythmias, CardiacHumansArrhythmiaAtrial fibrillationGene therapyGene transferSinus node dysfunctionVentricular tachycardia

Identifiers

PMID28642118
PMCPMC5546747
OpenAlexW2684689689

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.