Evidence map›Paper›PMID 32838054›Full record

ReviewCurrent opinion in endocrine and metabolic research2021

Subcellular hot spots of GPCR signaling promote vascular inflammation.

Cierra A Birch, Olivia Molinar-Inglis, JoAnn Trejo

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in endocrine and metabolic research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. GPCR Biased Signaling in Cancer.Handbook of experimental pharmacology · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Article
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  8. Role of G-protein coupled receptors in cardiovascular diseases.Frontiers in cardiovascular medicine · 2023
    Review
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  13. aPC/PAR1 confers endothelial anti-apoptotic activity via a discrete, β-arrestin-2-mediated SphK1-S1PR1-Akt signaling axis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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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

3 authors at 1 institution in 1 country.

Cierra A BirchDepartment of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, CA, 92093, USA.
Olivia Molinar-InglisDepartment of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, CA, 92093, USA.
JoAnn TrejoDepartment of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, CA, 92093, USA.
University of California San Diego · US

Funding

UCSD/SDSU IRACDAK12GM068524 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TREJO, JOANN · 2003 to 2025
$24.4M
Training In Cardiovascular Physiology & PharmacologyT32HL007444 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Ju Chen, Robert Scott Ross · 1985 to 2026
$11.1M
Cell Signaling by Protease-activated G Protein-coupled ReceptorsR35GM127121 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Joann Trejo · 2018 to 2026
$4.5M
NHLBI NIH HHS T32 HL007444NIGMS NIH HHS K12 GM068524NIGMS NIH HHS R35 GM127121
6 · The paper itself

Abstract

G-coupled protein receptors (GPCRs) comprise the largest class of druggable targets. Signaling by GPCRs is initiated from subcellular hot spots including the plasma membrane, signalosomes, and endosomes to contribute to vascular inflammation. GPCR-G protein signaling at the plasma membrane causes endothelial barrier disruption and also cross-talks with growth factor receptors to promote proinflammatory signaling. A second surge of GPCR signaling is initiated by cytoplasmic NFκB activation mediated by β-arrestins and CARMA-BCL10-MALT1 signalosomes. Once internalized, ubiquitinated GPCRs initiate signaling from endosomes via assembly of the transforming growth factor-β-activated kinase binding protein-1 (TAB1)-TAB2-p38 MAPK complex to promote vascular inflammation. Understanding the complexities of GPCR signaling is critical for development of new strategies to treat vascular inflammation such as that associated with COVID-19.

Indexed as

adherens junctions, AJangiotensin converting enzyme-2, ACE2angiotensin II type 1 receptor, AT1ArrestinsB-cell lymphoma protein 10, (BCL10)caspase recruitment domain-containing protein, CARMAcoronavirus disease of 2019, COVID-19COVID-19EndosomesEndothelialfibroblast-growth-factor, FGFG protein-coupled receptor, GPCRinhibitor of NFκB kinase, IKKJAK-STATJanus kinase, JAKMALT1mitogen-activated protein kinase, MAPKmucosa-associated lymphoid tissue lymphoma translocation protein 1, (MALT1)neural precursor cell expressed developmentally downregulated protein 4, NEDD4NFκBnuclear factor kappa-light-chain-enhancer of activated B cells, NFκBp38 MAPKplatelet activating factor, PAFprotease-activated receptor-1, PAR1severe acute respiratory syndrome coronavirus 2, SARS-CoV-2signal transducer and activator of transcription, STATtransforming growth factor-α-activated kinase binding protein-1, TAB1

Identifiers

PMID32838054
PMCPMC7431397
OpenAlexW3049603770

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.