Evidence map›Paper›PMID 29240722›Full record

ReviewInternational journal of molecular sciences2017

G Protein-Coupled Receptors at the Crossroad between Physiologic and Pathologic Angiogenesis: Old Paradigms and Emerging Concepts.

Ernestina M De Francesco, Federica Sotgia, Robert B Clarke, Michael P Lisanti, Marcello Maggiolini

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 20% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. The GPCR Connection: Linking Alzheimer's Disease and Glioblastoma.Journal of cellular and molecular medicine · 2026
    Review
  3. Article
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  17. AGGF1 Shows the α5β1 Integrin to Be AnotherArteriosclerosis, thrombosis, and vascular biology · 2021
    Article
  18. 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

5 authors at 3 institutions in 2 countries.

Ernestina M De FrancescoDepartment of Pharmacy, Health and Nutrition Sciences, University of Calabria via Savinio, 87036 Rende, Italy. ernestina.defrancesco@manchester.ac.uk.
Federica SotgiaTranslational Medicine, School of Environment and Life Sciences, Biomedical Research Centre, University of Salford, Greater Manchester M5 4WT, UK. fsotgia@gmail.com.
Robert B ClarkeBreast Cancer Now Research Unit, Division of Cancer Sciences, Manchester Cancer Research Centre, University of Manchester, Wilmslow Road, Manchester M20 4GJ, UK. robert.clarke@manchester.ac.uk.
Michael P LisantiTranslational Medicine, School of Environment and Life Sciences, Biomedical Research Centre, University of Salford, Greater Manchester M5 4WT, UK. michaelp.lisanti@gmail.com.
Marcello MaggioliniDepartment of Pharmacy, Health and Nutrition Sciences, University of Calabria via Savinio, 87036 Rende, Italy. marcellomaggiolini@yahoo.it.
Breast Cancer Now · GBUniversity of Salford · GBUniversity of Calabria · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G protein-coupled receptors (GPCRs) have been implicated in transmitting signals across the extra- and intra-cellular compartments, thus allowing environmental stimuli to elicit critical biological responses. As GPCRs can be activated by an extensive range of factors including hormones, neurotransmitters, phospholipids and other stimuli, their involvement in a plethora of physiological functions is not surprising. Aberrant GPCR signaling has been regarded as a major contributor to diverse pathologic conditions, such as inflammatory, cardiovascular and neoplastic diseases. In this regard, solid tumors have been demonstrated to activate an angiogenic program that relies on GPCR action to support cancer growth and metastatic dissemination. Therefore, the manipulation of aberrant GPCR signaling could represent a promising target in anticancer therapy. Here, we highlight the GPCR-mediated angiogenic function focusing on the molecular mechanisms and transduction effectors driving the patho-physiological vasculogenesis. Specifically, we describe evidence for the role of heptahelic receptors and associated G proteins in promoting angiogenic responses in pathologic conditions, especially tumor angiogenesis and progression. Likewise, we discuss opportunities to manipulate aberrant GPCR-mediated angiogenic signaling for therapeutic benefit using innovative GPCR-targeted and patient-tailored pharmacological strategies.

Indexed as

Signal TransductionAnimalsDisease ProgressionHumansModels, BiologicalNeoplasmsNeovascularization, PathologicNeovascularization, PhysiologicReceptors, G-Protein-CoupledReceptors, G-Protein-CoupledGPCRGPERHIF-1SDF-1sphingosine-1Ptumor angiogenesistumor microenvironmentVEGF

Identifiers

PMID29240722
PMCPMC5751314
OpenAlexW2772330573

What Socratic holds

Textmetadata
LicenceCC BY
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.