ArticleDrug discovery today. Therapeutic strategies2012
G protein-coupled Receptor Kinase 2 as a Therapeutic Target for Heart Failure.
Article in Drug discovery today. Therapeutic strategies, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Canonical or non-canonical, all aspects of G protein-coupled receptor kinase 2 in heart failure.Acta physiologica (Oxford, England) · 2025Review
- Unveiling the Role of GRK2: From Immune Regulation to Cancer Therapeutics.Mediators of inflammation · 2025Review
- Generation of Highly Selective, Potent, and Covalent G Protein-Coupled Receptor Kinase 5 Inhibitors.Journal of medicinal chemistry · 2021Article
- GRK5 - A Functional Bridge Between Cardiovascular and Neurodegenerative Disorders.Frontiers in pharmacology · 2018Review
- Article
- Adverse Effects on β-Adrenergic Receptor Coupling: Ischemic Postconditioning Failed to Preserve Long-Term Cardiac Function.Journal of the American Heart Association · 2017Article
- "Canonical and non-canonical actions of GRK5 in the heart".Journal of molecular and cellular cardiology · 2016Review
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
An ever-increasing number of people world-wide are developing and suffering from heart failure, and existing therapies, although improved are not ideal. Therefore, innovative treatment strategies are urgently needed. As our understanding of the underlying dysfunction of the myocardium increases, so does our ability to target the mechanisms responsible for heart failure progression. In this review we discuss novel molecular therapies and approaches for the treatment of heart failure. We will focus on the G protein-coupled receptor kinase GRK2, an increasing target for heart failure therapy, based on its important role in disease progression and the therapeutic potential of GRK2 inhibitors.
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.