Evidence map›Paper›PMID 29794115›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2018

nSMase2 (Type 2-Neutral Sphingomyelinase) Deficiency or Inhibition by GW4869 Reduces Inflammation and Atherosclerosis in Apoe

Tom Lallemand, Myriam Rouahi, Audrey Swiader, Marie-Hélène Grazide, Nancy Geoffre, Paul Alayrac, Emeline Recazens, Agnès Coste, Robert Salvayre, Anne Nègre-Salvayre and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
3.2field-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

79 citing papers in PubMed, 102 citations in OpenAlex.

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  11. From Genome to Geroscience: How DNA Damage Shapes Systemic Decline.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
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  19. Neutral sphingomyelinase 2: A promising drug target for CNS disease.Advances in pharmacology (San Diego, Calif.) · 2025
    Review
  20. Article

19 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Tom LallemandFrom the INSERM U-1048 Toulouse, France (T.L., M.R., A.S., M.-H.G., N.G., P.A., E.R., R.S., A.N.-S., N.A.).
Myriam RouahiFrom the INSERM U-1048 Toulouse, France (T.L., M.R., A.S., M.-H.G., N.G., P.A., E.R., R.S., A.N.-S., N.A.).
Audrey SwiaderFrom the INSERM U-1048 Toulouse, France (T.L., M.R., A.S., M.-H.G., N.G., P.A., E.R., R.S., A.N.-S., N.A.).
Marie-Hélène GrazideFrom the INSERM U-1048 Toulouse, France (T.L., M.R., A.S., M.-H.G., N.G., P.A., E.R., R.S., A.N.-S., N.A.).
Nancy GeoffreFrom the INSERM U-1048 Toulouse, France (T.L., M.R., A.S., M.-H.G., N.G., P.A., E.R., R.S., A.N.-S., N.A.).
Paul AlayracFrom the INSERM U-1048 Toulouse, France (T.L., M.R., A.S., M.-H.G., N.G., P.A., E.R., R.S., A.N.-S., N.A.).
Emeline RecazensFrom the INSERM U-1048 Toulouse, France (T.L., M.R., A.S., M.-H.G., N.G., P.A., E.R., R.S., A.N.-S., N.A.).
Agnès CostePHARMA-DEV, IRD UMR 152, Toulouse, France (A.C.).
Robert SalvayreFrom the INSERM U-1048 Toulouse, France (T.L., M.R., A.S., M.-H.G., N.G., P.A., E.R., R.S., A.N.-S., N.A.).
Anne Nègre-SalvayreFrom the INSERM U-1048 Toulouse, France (T.L., M.R., A.S., M.-H.G., N.G., P.A., E.R., R.S., A.N.-S., N.A.).
Nathalie AugéFrom the INSERM U-1048 Toulouse, France (T.L., M.R., A.S., M.-H.G., N.G., P.A., E.R., R.S., A.N.-S., N.A.) nathalie.auge@inserm.fr.
Université Toulouse III - Paul Sabatier · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAtherosclerosis is a chronic multifactorial and inflammatory disease of large and medium arteries and the leading cause of cardiovascular diseases worldwide. The aim of this study was to investigate whether and how the nSMase2 (type 2-neutral sphingomyelinase), a key enzyme of sphingolipid metabolism, may contribute to the development of atherosclerotic lesions. APPROACH AND

resultsThe role of nSMase2 in atherosclerosis was investigated in

conclusionsThe genetic deficiency or inhibition of nSMase2 strongly decreases the development of atherosclerotic lesions in

Indexed as

Aniline CompoundsAnimalsAnti-Inflammatory AgentsAortaAortic DiseasesAtherosclerosisBenzylidene CompoundsDisease Models, AnimalEndothelial CellsEnzyme InhibitorsInflammationInflammation MediatorsMacrophages, PeritonealMaleMiceMice, Inbred C57BLAniline CompoundsAnti-Inflammatory AgentsBenzylidene CompoundsEnzyme InhibitorsGW 4869Inflammation MediatorsNfe2l2 protein, mouseNF-E2-Related Factor 2Smpd3 protein, mouseSphingomyelin Phosphodiesteraseatherosclerosisendothelial cellsinflammationmacrophagessphingolipids

Identifiers

PMID29794115
PMCPMC6039418
OpenAlexW2804321542

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.