ArticleMolecular and cellular biochemistry2004
Genetic and phenotypic targeting of β-adrenergic signaling in heart failure.
Article in Molecular and cellular biochemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed.
- Interplay between variability in intrinsic cellular properties and heart failure-associated remodeling in a simulated population with human heart failure.Journal of molecular and cellular cardiology · 2026Article
- Protein kinase Cα as a heart failure therapeutic target.Journal of molecular and cellular cardiology · 2011Review
- Regulation of Ryanodine Receptor Ion Channels Through Posttranslational Modifications.Current topics in membranes · 2010Article
- In situ molecular level studies on membrane related peptides and proteins in real time using sum frequency generation vibrational spectroscopy.Journal of structural biology · 2009Review
- Kinase activity-independent regulation of cyclin pathway by GRK2 is essential for zebrafish early development.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Inhibition of vascular smooth muscle G protein-coupled receptor kinase 2 enhances alpha1D-adrenergic receptor constriction.American journal of physiology. Heart and circulatory physiology · 2008Article
- Endogenous Gs-coupled receptors in smooth muscle exhibit differential susceptibility to GRK2/3-mediated desensitization.Biochemistry · 2008Article
- A GRK5 polymorphism that inhibits beta-adrenergic receptor signaling is protective in heart failure.Nature medicine · 2008Article
- Beta-adrenergic receptor signaling in cardiac function and heart failure.McGill journal of medicine : MJM : an international forum for the advancement of medical sciences by students · 2007Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure is a leading cause of hospitalization worldwide. No major significant improvements in prognosis have been achieved for heart failure over the last several decades despite advances in disease management. Heart failure itself represents a final common endpoint for several disease entities, including hypertension and coronary artery disease. On a molecular level, certain biochemical features remain common to failing myocardium. Among these are alterations in the β-adrenergic receptor (β-AR) signaling cascade. Recent advances in transgenic and gene therapy techniques have presented novel therapeutic strategies for management of heart failure via genetic manipulation of β-AR signaling including the targeted inhibition of the β-AR kinase (βARK1 or GRK2). In this review, we will discuss the β-AR signaling changes that accompany heart failure as well as corresponding therapeutic strategies. We will then review the evidence from transgenic mouse work supporting the use of β-AR manipulation in the failing heart and more recent in vivo applications of gene therapy directed at reversing or preventing heart failure. (Mol Cell Biochem 263: 5-9, 2004).
Indexed as
Identifiers
27520660What 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.