ReviewThe Journal of physiology2003
Targeting calcium cycling proteins in heart failure through gene transfer.
Review in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 96 citations in OpenAlex.
- Antenatal Glucocorticoid Administration Promotes Cardiac Structure and Energy Metabolism Maturation in Preterm Fetuses.International journal of molecular sciences · 2022Review
- AKAP18δ Anchors and Regulates CaMKII Activity at Phospholamban-SERCA2 and RYR.Circulation research · 2022Article
- Cell death in the pathogenesis and progression of heart failure.Heart failure reviews · 2016Article
- Cytosolic H2O2 mediates hypertrophy, apoptosis, and decreased SERCA activity in mice with chronic hemodynamic overload.American journal of physiology. Heart and circulatory physiology · 2014Article
- The role of CaMKII regulation of phospholamban activity in heart disease.Frontiers in pharmacology · 2014Review
- SERCA2a gene therapy in heart failure: an anti-arrhythmic positive inotrope.British journal of pharmacology · 2014Review
- High-throughput FRET assay yields allosteric SERCA activators.Journal of biomolecular screening · 2013Article
- Short-term akt activation in cardiac muscle cells improves contractile function in failing hearts.The American journal of pathology · 2012Article
- Concomitant intravenous nitroglycerin with intracoronary delivery of AAV1.SERCA2a enhances gene transfer in porcine hearts.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
- Striated muscle tropomyosin isoforms differentially regulate cardiac performance and myofilament calcium sensitivity.Journal of muscle research and cell motility · 2010Article
- Investigations into tropomyosin function using mouse models.Journal of molecular and cellular cardiology · 2010Review
- Targeted SERCA2a gene expression identifies molecular mechanism and therapeutic target for arrhythmogenic cardiac alternans.Circulation. Arrhythmia and electrophysiology · 2009Article
- Role of xanthine oxidoreductase in cardiac nitroso-redox imbalance.Frontiers in bioscience (Landmark edition) · 2009Review
- Molecular cardiology in translation: gene, cell and chemical-based experimental therapeutics for the failing heart.Journal of cardiovascular translational research · 2008Review
- Intracellular devastation in heart failure.Heart failure reviews · 2008Review
- Advances in gene-based therapy for heart failure.Journal of cardiovascular translational research · 2008Review
- The Ca2+ ATPase of cardiac sarcoplasmic reticulum: Physiological role and relevance to diseases.Biochemical and biophysical research communications · 2008Review
- Effects of levosimendan on cardiac remodeling and cardiomyocyte apoptosis in hypertensive Dahl/Rapp rats.British journal of pharmacology · 2007Article
- Regulation of phosphodiesterase 3 and inducible cAMP early repressor in the heart.Circulation research · 2007Review
- Heart failure: a model of cardiac and skeletal muscle energetic failure.Pflugers Archiv : European journal of physiology · 2006Review
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 2 institutions in 1 country.
Funding
Abstract
Our understanding of cardiac excitation-contraction coupling has improved significantly over the last 10 years. Furthermore, defects in the various steps of excitation-contraction coupling that characterize cardiac dysfunction have been identified in human and experimental models of heart failure. The various abnormalities in ionic channels, transporters, kinases and various signalling pathways collectively contribute to the 'failing phenotype.' However, deciphering the causative changes continues to be a challenge. An important tool in dissecting the importance of the various changes in heart failure has been the use of cardiac gene transfer. To achieve effective cardiac gene transfer a number of obstacles remain, including appropriate vectors for gene delivery, appropriate delivery systems, and a better understanding of the biology of the disease. In this review, we will examine our current understanding of these various factors. Gene transfer provides not only a potential therapeutic modality but also an approach to identifying and validating molecular targets.
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.