Evidence map›Paper›PMID 19434053›Full record

ReviewCurrent opinion in nephrology and hypertension2009

Vascular signaling through G protein-coupled receptors: new concepts.

Masuko Ushio-Fukai

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.7field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 64 citations in OpenAlex.

  1. Trial
  2. Review
  3. Pro-inflammatory cytokines disruptFrontiers in endocrinology · 2025
    Article
  4. Review
  5. Review
  6. Article
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  14. Nitrosative stress uncovers potent βAmerican journal of physiology. Heart and circulatory physiology · 2018
    Article
  15. Article
  16. Review
  17. Experimental evaluation of the generalized vibrational theory of G protein-coupled receptor activation.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Masuko Ushio-FukaiDepartment of Pharmacology, Center for Lung and Vascular Biology, Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, Illinois 60612, USA. mfukai@uic.edu
University of Illinois Chicago · US

Funding

Reactive Oxygen Species and Endothelial MigrationR01HL077524 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI USHIO-FUKAI, MASUKO · 2006 to 2010
$2.2M
NHLBI NIH HHS R01 HL077524
6 · The paper itself

Abstract

purpose of reviewG protein-coupled receptor (GPCR) signaling machinery can serve as a direct target of reactive oxygen species (ROS), including superoxide (O2-), hydrogen peroxide (H2O2) as well as reactive nitrogen species, including nitric oxide and S-nitrosothiols (SNOs). Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is one of the major sources of O2- produced following GPCR activation in vasculature. Nitric oxide is generated by three isoforms of nitric oxide synthase (NOS). This review will summarize the recent progress on GPCR signaling modulation by NADPH oxidase-derived ROS and NOS-derived SNOs. RECENT

findingsROS and reactive nitrogen species play an important role in GPCR signaling involved in various physiological functions such as cell growth, migration, gene expression as well as pathophysiologies. NADPH oxidase-derived ROS activate specific redox signaling events involved in cardiovascular diseases. SNOs can modulate GPCR signaling and internalization through S-nitrosylation of the scaffolding protein beta-arrestin, the GPCR kinases, and dynamin, a guanosine triphosphatase responsible for endocytosis. SUMMARY: NADPH oxidase-derived ROS and NOS-derived SNOs are now recognized as important second messengers to regulate GPCR signaling, thereby contributing to various biological and pathophysiological functions. Understanding the molecular mechanism of how ROS, nitric oxide, and SNOs might modulate GPCR signaling is essential for development of novel therapeutic approaches.

Indexed as

AnimalsArrestinsbeta-ArrestinsDynaminsG-Protein-Coupled Receptor Kinase 2HumansMuscle, Smooth, VascularNitric Oxide SynthaseReactive Oxygen SpeciesReceptor, Angiotensin, Type 1Receptors, G-Protein-CoupledSignal TransductionS-NitrosothiolsArrestinsbeta-ArrestinsDynaminsG-Protein-Coupled Receptor Kinase 2GRK2 protein, humanNitric Oxide SynthaseReactive Oxygen SpeciesReceptor, Angiotensin, Type 1Receptors, G-Protein-CoupledS-Nitrosothiols

Identifiers

PMID19434053
PMCPMC2892476
OpenAlexW2074496362

What OpenQuestion holds

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Registered trials

None linked

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.