ReviewGene therapy2012
Targeting GRK2 by gene therapy for heart failure: benefits above β-blockade.
Review in Gene therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 29 citations in OpenAlex.
- G-Protein-Coupled Receptor Kinase 2 Limits CCL21-Induced T Cell Migration via Phospholipase Cγ1.Receptors (Basel, Switzerland) · 2025Article
- Unveiling the Role of GRK2: From Immune Regulation to Cancer Therapeutics.Mediators of inflammation · 2025Review
- Heartfelt Breakthroughs: Elevating Quality of Life with Cutting-Edge Advances in Heart Failure Treatment.Journal of cardiovascular development and disease · 2024Review
- Chronic Sympathetic Hyperactivity Triggers Electrophysiological Remodeling and Disrupts Excitation-Contraction Coupling in Heart.Scientific reports · 2020Article
- Is GRK2 a new target for cardiovascular disease?Hypertension research : official journal of the Japanese Society of Hypertension · 2018Article
- Article
- Therapeutic Targets for Treatment of Heart Failure: Focus on GRKs and β-Arrestins Affecting βAR Signaling.Frontiers in pharmacology · 2018Review
- Gene therapy for the treatment of heart failure: promise postponed.European heart journal · 2016Review
- Modeling the effects of β1-adrenergic receptor blockers and polymorphisms on cardiac myocyte Ca2+ handling.Molecular pharmacology · 2014Article
- A compartmentalized mathematical model of the β1-adrenergic signaling system in mouse ventricular myocytes.PloS one · 2014Article
- Structural and functional plasticity in long-term cultures of adult ventricular myocytes.Journal of molecular and cellular cardiology · 2013Article
- GRK 2 level in peripheral blood lymphocytes of elderly patients with acute myocardial infarction.Journal of geriatric cardiology : JGC · 2013Article
- Pathological ventricular remodeling: therapies: part 2 of 2.Circulation · 2013Article
- Gene targeting in ischemic heart disease and failure: translational and clinical studies.Biochemical pharmacology · 2013Review
- AAV-mediated gene therapy for heart failure: enhancing contractility and calcium handling.F1000prime reports · 2013Article
- Altered sarcoplasmic reticulum calcium cycling--targets for heart failure therapy.Nature reviews. Cardiology · 2012Review
- G protein-coupled Receptor Kinase 2 as a Therapeutic Target for Heart Failure.Drug discovery today. Therapeutic strategies · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure (HF) is a common pathological end point for several cardiac diseases. Despite reasonable achievements in pharmacological, electrophysiological and surgical treatments, prognosis for chronic HF remains poor. Modern therapies are generally symptom oriented and do not currently address specific intracellular molecular signaling abnormalities. Therefore, new and innovative therapeutic approaches are warranted and, ideally, these could at least complement established therapeutic options if not replace them. Gene therapy has potential to serve in this regard in HF as vectors can be directed toward diseased myocytes and directly target intracellular signaling abnormalities. Within this review, we will dissect the adrenergic system contributing to HF development and progression with special emphasis on G-protein-coupled receptor kinase 2 (GRK2). The levels and activity of GRK2 are increased in HF and we and others have demonstrated that this kinase is a major molecular culprit in HF. We will cover the evidence supporting gene therapy directed against myocardial as well as adrenal GRK2 to improve the function and structure of the failing heart and how these strategies may offer complementary and synergistic effects with the existing HF mainstay therapy of β-adrenergic receptor antagonism.
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.