Evidence map›Paper›PMID 34615374›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2021

Inhibition of Vascular Growth by Modulation of the Anandamide/Fatty Acid Amide Hydrolase Axis.

Sarah Rieck, Sofia Kilgus, Johanna H Meyer, Hao Huang, Lan Zhao, Michaela Matthey, Xin Wang, Steffen Schmitz-Valckenberg, Bernd K Fleischmann, Daniela Wenzel

Open access · hybridAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

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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

10 authors at 4 institutions in 2 countries.

Sarah Rieck *Institute of Physiology I, Life&Brain Center, Medical Faculty (S.R., S.K., B.K.F., D.W.), University of Bonn, Germany.
Sofia Kilgus *Institute of Physiology I, Life&Brain Center, Medical Faculty (S.R., S.K., B.K.F., D.W.), University of Bonn, Germany.
Johanna H MeyerDepartment of Ophthalmology (J.H.M., S.S.-V.), University of Bonn, Germany.
Hao HuangDepartment of Biomedical Sciences, City University of Hong Kong (H.H., L.Z., X.W.).
Lan ZhaoDepartment of Biomedical Sciences, City University of Hong Kong (H.H., L.Z., X.W.).ORCID 0000-0003-2681-7695
Michaela MattheyDepartment of Systems Physiology, Institute of Physiology, Medical Faculty, Ruhr University of Bochum, Germany (M.M., D.W.).
Xin WangDepartment of Biomedical Sciences, City University of Hong Kong (H.H., L.Z., X.W.).
Steffen Schmitz-ValckenbergDepartment of Ophthalmology (J.H.M., S.S.-V.), University of Bonn, Germany.ORCID 0000-0003-3358-9942
Bernd K FleischmannInstitute of Physiology I, Life&Brain Center, Medical Faculty (S.R., S.K., B.K.F., D.W.), University of Bonn, Germany.ORCID 0000-0002-9202-8363
Daniela WenzelInstitute of Physiology I, Life&Brain Center, Medical Faculty (S.R., S.K., B.K.F., D.W.), University of Bonn, Germany.ORCID 0000-0003-1100-6363
Life & Brain (Germany) · DECity University of Hong Kong · HKUniversity of Bonn · DERuhr University Bochum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePathological angiogenesis is a hallmark of various diseases characterized by local hypoxia and inflammation. These disorders can be treated with inhibitors of angiogenesis, but current compounds display a variety of side effects and lose efficacy over time. This makes the identification of novel signaling pathways and pharmacological targets involved in angiogenesis a top priority. Approach and Results: Here, we show that inactivation of FAAH (fatty acid amide hydrolase), the enzyme responsible for degradation of the endocannabinoid anandamide, strongly impairs angiogenesis in vitro and in vivo. Both, the pharmacological FAAH inhibitor URB597 and anandamide induce downregulation of gene sets for cell cycle progression and DNA replication in endothelial cells. This is underscored by cell biological experiments, in which both compounds inhibit proliferation and migration and evoke cell cycle exit of endothelial cells. This prominent antiangiogenic effect is also of pathophysiological relevance in vivo, as laser-induced choroidal neovascularization in the eye of

conclusionsThus, elevation of endogenous anandamide levels by FAAH inhibition represents a novel antiangiogenic mechanism.

Indexed as

AmidohydrolasesAnimalsArachidonic AcidsBlood VesselsCannabinoid Receptor AgonistsCattleCell LineDisease Models, AnimalEndocannabinoidsEndothelium, VascularFatty Acid Amide HydrolasesHumansMiceMuscle, Smooth, VascularNeovascularization, PathologicPolyunsaturated AlkamidesAmidohydrolasesanandamideArachidonic AcidsCannabinoid Receptor AgonistsEndocannabinoidsFatty Acid Amide HydrolasesPolyunsaturated Alkamidesanandamidechoroidal neovascularizationendothelial cellfatty acid amide hydrolaseinflammation

Identifiers

PMID34615374
PMCPMC8608012
OpenAlexW3202098702

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.