Evidence map›Paper›PMID 31974349›Full record

ArticleCell death & disease2020

Effects of thrombospondin-4 on pro-inflammatory phenotype differentiation and apoptosis in macrophages.

Mohammed Tanjimur Rahman, Santoshi Muppala, Jiahui Wu, Irene Krukovets, Dmitry Solovjev, Dmitriy Verbovetskiy, Chioma Obiako, Edward F Plow, Olga Stenina-Adognravi

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

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  13. Pathophysiological roles of thrombospondin-4 in disease development.Seminars in cell & developmental biology · 2024
    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

9 authors at 1 institution in 1 country.

Mohammed Tanjimur RahmanDepartment of Cardiovascular & Metabolic Sciences, Cleveland Clinic, Cleveland, OH, USA.ORCID http://orcid.org/0000-0002-9790-0069
Santoshi MuppalaDepartment of Cardiovascular & Metabolic Sciences, Cleveland Clinic, Cleveland, OH, USA.
Jiahui WuDepartment of Cardiovascular & Metabolic Sciences, Cleveland Clinic, Cleveland, OH, USA.
Irene KrukovetsDepartment of Cardiovascular & Metabolic Sciences, Cleveland Clinic, Cleveland, OH, USA.
Dmitry SolovjevDepartment of Cardiovascular & Metabolic Sciences, Cleveland Clinic, Cleveland, OH, USA.
Dmitriy VerbovetskiyDepartment of Cardiovascular & Metabolic Sciences, Cleveland Clinic, Cleveland, OH, USA.
Chioma ObiakoDepartment of Cardiovascular & Metabolic Sciences, Cleveland Clinic, Cleveland, OH, USA.
Edward F PlowDepartment of Cardiovascular & Metabolic Sciences, Cleveland Clinic, Cleveland, OH, USA.
Olga Stenina-AdognraviDepartment of Cardiovascular & Metabolic Sciences, Cleveland Clinic, Cleveland, OH, USA. stenino@ccf.org.ORCID http://orcid.org/0000-0002-1256-0545
Cleveland Clinic · US

Funding

TSP-4 genetic variants in atherogenesis and angiogenesisR01HL117216 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI PLOW, EDWARD FRANKLIN, STENINA, OLGA I · 2013 to 2017
$1.9M
Tissue Specific Regulation of Diabetes-Associated Cancer GrowthR01CA177771 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI STENINA, OLGA I · 2014 to 2018
$1.6M
NCI NIH HHS R01 CA177771NHLBI NIH HHS R01 HL117216
6 · The paper itself

Abstract

Thrombospondin-4 (TSP-4) attracted renewed attention recently as a result of assignment of new functions to this matricellular protein in cardiovascular, muscular, and nervous systems. We have previously reported that TSP-4 promotes local vascular inflammation in a mouse atherosclerosis model. A common variant of TSP-4, P387-TSP-4, was associated with increased cardiovascular disease risk in human population studies. In a mouse atherosclerosis model, TSP-4 had profound effect on accumulation of macrophages in lesions, which prompted us to examine its effects on macrophages in more detail. We examined the effects of A387-TSP-4 and P387-TSP-4 on mouse macrophages in cell culture and in vivo in the model of LPS-induced peritonitis. In tissues and in cell culture, TSP-4 expression was associated with inflammation: TSP-4 expression was upregulated in peritoneal tissues in LPS-induced peritonitis, and pro-inflammatory signals, INFγ, GM-CSF, and LPS, induced TSP-4 expression in macrophages in vivo and in cell culture. Deficiency in TSP-4 in macrophages from Thbs4

Indexed as

ApoptosisAnimalsBiomarkersCell SurvivalCytokinesInflammationInflammation MediatorsLipopolysaccharidesMacrophages, PeritonealMiceMice, Inbred C57BLMonocytesPeritonitisPhenotypePhosphorylationRAW 264.7 CellsBiomarkersCytokinesInflammation MediatorsLipopolysaccharidesRecombinant Proteinsthrombospondin 4Thrombospondins

Identifiers

PMID31974349
PMCPMC6978349
OpenAlexW3001436233

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.