ArticleThe Journal of clinical investigation1998
Enhancement of murine cardiac chronotropy by the molecular transfer of the human beta2 adrenergic receptor cDNA.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 126 citations in OpenAlex.
- Review
- Harnessing cell reprogramming for cardiac biological pacing.Journal of biomedical science · 2023Review
- Implementing Biological Pacemakers: Design Criteria for Successful.Circulation. Arrhythmia and electrophysiology · 2021Review
- Bioengineering the Cardiac Conduction System: Advances in Cellular, Gene, and Tissue Engineering for Heart Rhythm Regeneration.Frontiers in bioengineering and biotechnology · 2021Review
- Article
- Insulin gene enhancer binding protein 1 induces adipose tissue‑derived stem cells to differentiate into pacemaker‑like cells.International journal of molecular medicine · 2019Article
- Gene Therapy Approaches to Biological Pacemakers.Journal of cardiovascular development and disease · 2018Review
- Next-generation pacemakers: from small devices to biological pacemakers.Nature reviews. Cardiology · 2018Review
- Gene therapy to treat cardiac arrhythmias.Nature reviews. Cardiology · 2015Review
- Stem cell therapy for electrophysiological disorders.Current cardiology reports · 2013Review
- Reprogramming paces the heart.Nature biotechnology · 2013Article
- Ca(2+)-stimulated adenylyl cyclase AC1 generates efficient biological pacing as single gene therapy and in combination with HCN2.Circulation · 2012Article
- The road to biological pacing.Nature reviews. Cardiology · 2011Review
- Regenerative therapies in electrophysiology and pacing: introducing the next steps.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2011Review
- Gene therapy strategies for cardiac electrical dysfunction.Journal of molecular and cellular cardiology · 2011Review
- The cardiac conduction system.Circulation · 2011Review
- Use of rats mesenchymal stem cells modified with mHCN2 gene to create biologic pacemakers.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2010Article
- Biological therapies for cardiac arrhythmias: can genes and cells replace drugs and devices?Circulation research · 2010Review
- Coupling an HCN2-expressing cell to a myocyte creates a two-cell pacing unit.The Journal of physiology · 2009Article
- Molecular mechanisms of inherited arrhythmias.Current genomics · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac pacemaking offers a unique opportunity for direct gene transfer into the heart. An experimental system was developed to assay the effects of transferring the human beta2 adrenergic receptor (beta2AR) under in vitro, ex vivo, and finally in vivo conditions. Constructs encoding either beta2AR or LacZ were used in chronotropy studies with isolated myocytes, and transplanted as well as endogenous murine hearts. Murine embryonic cardiac myocytes were transiently transfected with plasmid constructs. The total percentage of myocytes spontaneously contracting was greater in beta2AR transfected cells, as compared with control cells (67 vs. 42+/-5%). In addition, the percentage of myocytes with chronotropic rates > 60 beats per minute (bpm) was higher in the beta2AR population, as compared with control cells (37 vs. 15+/-5%). The average contractile rate was greater in the beta2AR transfected myocytes at baseline (71+/-14 vs. 50+/-10 bpm; P < 0.001) as well as with the addition of 10(-)3 M isoproterenol (98+/-26 vs. 75+/-18 bpm; P < 0.05). Based on these results, a murine neonatal cardiac transplantation model was used to study the ex vivo effects of targeted expression of beta2AR. The constructs were transfected into the right atrium of transplanted hearts. Injection of the beta2AR construct increased the heart rate by approximately 40% (224+/-37 vs. 161+/-42 bpm; P < 0.005). Finally, the constructs were tested in vivo with injection into the right atrium of the endogenous heart. These results were similar to the ex vivo data with injection of the beta2AR constructs increasing the endogenous heart rates by approximately 40%, as compared with control injected hearts (550+/-42 vs. 390+/-37 bpm; P < 0.05). These studies demonstrate that local targeting of gene expression may be a feasible modality to regulate the cardiac pacemaking activity.
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.