ReviewInternational journal of molecular sciences2013
βArrestins in cardiac G protein-coupled receptor signaling and function: partners in crime or "good cop, bad cop"?
Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 27 citations in OpenAlex.
- β-Adrenergic Receptors: Not Always Outside-In.Physiology (Bethesda, Md.) · 2026Review
- Adrenoceptor Desensitization: Current Understanding of Mechanisms.Pharmacological reviews · 2024Review
- GTPγS Assay for Measuring Agonist-Induced Desensitization of Two Human Polymorphic AlphaMethods in molecular biology (Clifton, N.J.) · 2022Article
- β-Adrenergic receptor, an essential target in cardiovascular diseases.Heart failure reviews · 2020Review
- Not all arrestins are created equal: Therapeutic implications of the functional diversity of the β-arrestins in the heart.World journal of cardiology · 2019Article
- G Protein-Coupled Receptor Signaling Through β-Arrestin-Dependent Mechanisms.Journal of cardiovascular pharmacology · 2017Review
- Adaptive Activation of a Stress Response Pathway Improves Learning and Memory Through Gs and β-Arrestin-1-Regulated Lactate Metabolism.Biological psychiatry · 2017Article
- Angiotensin receptor blocker drugs and inhibition of adrenal beta-arrestin-1-dependent aldosterone production: Implications for heart failure therapy.World journal of cardiology · 2017Article
- Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling.Nature communications · 2017Article
- Regulation of podocyte lesions in diabetic nephropathy via miR-34a in the Notch signaling pathway.Medicine · 2016Article
- Molecular switches under TGFβ signalling during progression from cardiac hypertrophy to heart failure.British journal of pharmacology · 2016Review
- Loss of β-arrestin1 expression predicts unfavorable prognosis for non-small cell lung cancer patients.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Adrenal G protein-coupled receptor kinase-2 in regulation of sympathetic nervous system activity in heart failure.World journal of cardiology · 2015Review
- Heart failure-specific changes in protein kinase signalling.Pflugers Archiv : European journal of physiology · 2014Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
βArrestin (βarr)-1 and -2 (βarrs) (or Arrestin-2 and -3, respectively) are universal G protein-coupled receptor (GPCR) adapter proteins expressed abundantly in extra-retinal tissues, including the myocardium. Both were discovered in the lab of the 2012 Nobel Prize in Chemistry co-laureate Robert Lefkowitz, initially as terminators of signaling from the β-adrenergic receptor (βAR), a process known as functional desensitization. They are now known to switch GPCR signaling from G protein-dependent to G protein-independent, which, in the case of βARs and angiotensin II type 1 receptor (AT1R), might be beneficial, e.g., anti-apoptotic, for the heart. However, the specific role(s) of each βarr isoform in cardiac GPCR signaling and function (or dysfunction in disease), remain unknown. The current consensus is that, whereas both βarr isoforms can desensitize and internalize cardiac GPCRs, they play quite different (even opposing in certain instances) roles in the G protein-independent signaling pathways they initiate in the cardiovascular system, including in the myocardium. The present review will discuss the current knowledge in the field of βarrs and their roles in GPCR signaling and function in the heart, focusing on the three most important, for cardiac physiology, GPCR types (β1AR, β2AR & AT1R), and will also highlight important questions that currently remain unanswered.
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.