Evidence map›Paper›PMID 23479425›Full record

ArticleJournal of lipid research2013

Endogenous cannabinoid receptor CB1 activation promotes vascular smooth-muscle cell proliferation and neointima formation.

Filippo Molica, Fabienne Burger, Aurélien Thomas, Christian Staub, Anne Tailleux, Bart Staels, Graziano Pelli, Andreas Zimmer, Benjamin Cravatt, Christian M Matter and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  5. Role of Cannabinoid Signaling in Cardiovascular Function and Ischemic Injury.The Journal of pharmacology and experimental therapeutics · 2023
    Review
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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

12 authors at 8 institutions in 5 countries.

Filippo MolicaDivision of Cardiology, University Hospital, Geneva, Switzerland.
Fabienne Burger
Aurélien Thomas
Christian Staub
Anne Tailleux
Bart Staels
Graziano Pelli
Andreas Zimmer
Benjamin Cravatt
Christian M Matter
Pal Pacher
Sabine Steffens
University Hospital of Geneva · CHEuropean Genomic Institute for Diabetes · FRUniversity Centre of Legal Medicine · CHLudwig-Maximilians-Universität München · DENational Institutes of Health · USScripps Research Institute · USUniversity of Bonn · DEUniversity of Zurich · CH

Funding

Mechanism of oxidative/nitrosative stress and inflammation-induced tissue injuryZIAAA000375 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI PACHER, PAL · 2009 to 2025
$27.8M
6 · The paper itself

Abstract

Percutaneous transluminal angioplasty is frequently used in patients with severe arterial narrowing due to atherosclerosis. However, it induces severe arterial injury and an inflammatory response leading to restenosis. Here, we studied a potential activation of the endocannabinoid system and the effect of FA amide hydrolase (FAAH) deficiency, the major enzyme responsible for endocannabinoid anandamide degradation, in arterial injury. We performed carotid balloon injury in atherosclerosis-prone apoE knockout (apoE(-/-)) and apoE(-/-)FAAH(-/-) mice. Anandamide levels were systemically elevated in apoE(-/-) mice after balloon injury. ApoE(-/-)FAAH(-/-) mice had significantly higher baseline anandamide levels and enhanced neointima formation compared with apoE(-/-) controls. The latter effect was inhibited by treatment with CB1 antagonist AM281. Similarly, apoE(-/-) mice treated with AM281 had reduced neointimal areas, reduced lesional vascular smooth-muscle cell (SMC) content, and proliferating cell counts. The lesional macrophage content was unchanged. In vitro proliferation rates were significantly reduced in CB1(-/-) SMCs or when treating apoE(-/-) or apoE(-/-)FAAH(-/-) SMCs with AM281. Macrophage in vitro adhesion and migration were marginally affected by CB1 deficiency. Reendothelialization was not inhibited by treatment with AM281. In conclusion, endogenous CB1 activation contributes to vascular SMC proliferation and neointima formation in response to arterial injury.

Indexed as

AmidohydrolasesAnimalsApolipoproteins EAtherosclerosisCell ProliferationFatty Acid Amide HydrolasesHumansMiceMice, KnockoutMorpholinesMuscle, Smooth, VascularNeointimaPyrazolesReceptor, Cannabinoid, CB1Tunica IntimaAM 281AmidohydrolasesApolipoproteins EFatty Acid Amide HydrolasesMorpholinesPyrazolesReceptor, Cannabinoid, CB1

Identifiers

PMID23479425
PMCPMC3622330
OpenAlexW2171047361

What OpenQuestion 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 OpenQuestion graph.