Evidence map›Paper›PMID 30910852›Full record

ArticleBioscience reports2019

Inhibition of acid sphingomyelinase activity ameliorates endothelial dysfunction in

Meng Jiang, Shanya Huang, Wang Duan, Qiaoshu Liu, Minxiang Lei

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

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  14. Acid sphingomyelinase promotes SGK1-dependent vascular calcification.Clinical science (London, England : 1979) · 2021
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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 1 institution in 1 country.

Meng JiangXiangya Hospital of Central South University, Hunan Province, Xiangya Street 78, Changsha 410008, China.
Shanya HuangXiangya Hospital of Central South University, Hunan Province, Xiangya Street 78, Changsha 410008, China.
Wang DuanXiangya Hospital of Central South University, Hunan Province, Xiangya Street 78, Changsha 410008, China.
Qiaoshu LiuXiangya Hospital of Central South University, Hunan Province, Xiangya Street 78, Changsha 410008, China.
Minxiang LeiXiangya Hospital of Central South University, Hunan Province, Xiangya Street 78, Changsha 410008, China leiminxiang@gmail.com.ORCID 0000-0003-1702-5952
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acid sphingomyelinase (aSMase) plays an important role in endothelial dysfunction. Here, we show that elevated aSMase activity and ceramide content were reduced by desipramine treatment in diabetic animals. The inhibitor of aSMase, desipramine, improved vascular dysfunction in db/db mice. High glucose (HG)-induced up-regulation of aSMase activity and ceramide levels were restored by treatment with aSMase siRNA or desipramine in endothelial cells. In addition, aSMase siRNA or desipramine treatment increased the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in diabetic mouse aortas and aortic endothelial cells with HG.These results indicate that inhibition of aSMase/ceramide pathway improves endothelium-dependent vascular relaxation (EDR) largely through regulating the eNOS/NO pathway in diabetic animals.

Indexed as

AnimalsCells, CulturedCeramidesDiabetes Mellitus, ExperimentalEndothelium, VascularMaleMiceMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIIRatsSignal TransductionSphingomyelin PhosphodiesteraseASMase, mouseCeramidesNitric OxideNitric Oxide Synthase Type IIISphingomyelin Phosphodiesteraseacid sphingomyelinaseceramidediabetesendothelial dysfunction

Identifiers

PMID30910852
PMCPMC6481240
OpenAlexW2942045465

What OpenQuestion 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 OpenQuestion graph.