Evidence map›Paper›PMID 32497259›Full record

ArticleBritish journal of pharmacology2020

Recombinant thrombomodulin protects against LPS-induced acute respiratory distress syndrome via preservation of pulmonary endothelial glycocalyx.

Kodai Suzuki, Hideshi Okada, Genzou Takemura, Chihiro Takada, Hiroyuki Tomita, Hirohisa Yano, Isamu Muraki, Ryogen Zaikokuji, Ayumi Kuroda, Hirotsugu Fukuda and 13 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

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  16. Advances in Biomarkers for Diagnosis and Treatment of ARDS.Diagnostics (Basel, Switzerland) · 2023
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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

23 authors at 3 institutions in 1 country.

Kodai SuzukiDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Hideshi OkadaDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.ORCID 0000-0002-7775-4308
Genzou TakemuraDepartment of Internal Medicine, Asahi University School of Dentistry, Mizuho, Japan.
Chihiro TakadaDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Hiroyuki TomitaDepartment of Tumour Pathology, Gifu University Graduate School of Medicine, Gifu, Japan.ORCID 0000-0002-3291-0274
Hirohisa YanoDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Isamu MurakiDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Ryogen ZaikokujiDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Ayumi KurodaDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Hirotsugu FukudaDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Ayane NishioDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Shigeo TakashimaDivision of Genomics Research, Life Science Research Center, Gifu University, Gifu, Japan.
Akio SuzukiDepartment of Pharmacy, Gifu University Hospital, Gifu, Japan.
Nagisa MiyazakiDepartment of Internal Medicine, Asahi University School of Dentistry, Mizuho, Japan.
Tetsuya FukutaDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Noriaki YamadaDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Takatomo WatanabeDivision of Clinical Laboratory, Gifu University Hospital, Gifu, Japan.
Tomoaki DoiDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Takahiro YoshidaDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Keisuke KumadaDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Hiroaki UshikoshiDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Shozo YoshidaDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Shinji OguraDepartment of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan.
Gifu University · JPAsahi University · JPGifu University Hospital · JP

Funding

Asahi Kasei Pharma CorporationJapan Society for the Promotion of Science 15K10973Japan Society for the Promotion of Science 16H05497Japan Society for the Promotion of Science 16K09509Japan Society for the Promotion of Science 16K20381Japan Society for the Promotion of Science 17K11569Japan Society for the Promotion of Science 18K08884Japan Society for the Promotion of Science 18K08914Japan Society for the Promotion of Science 18K16511Japan Society for the Promotion of Science 19H03756Japan Society for the Promotion of Science 19K09410Japan Society for the Promotion of Science 19K18347
6 · The paper itself

Abstract

background and purposeDisruption of the endothelial glycocalyx is causally related to microvascular endothelial dysfunction, a characteristic of sepsis-induced acute respiratory distress syndrome (ARDS). Recombinant human thrombomodulin (rhTM) attenuates vascular endothelial injuries, but the underlying mechanism remains elusive. Here, we investigated the structural basis and molecular mechanisms of rhTM effects on vascular endothelial injury in a model of sepsis. EXPERIMENTAL APPROACH: LPS (20 mg·kg KEY

resultsSurvival rate of rhTM-treated mice was significantly higher than that of control mice 48 h after LPS injection. Serum concentrations of IL-6 and high-mobility group box 1 were lower in the rhTM-treated group than in the control. Injury to the endothelial glycocalyx in pulmonary capillaries was attenuated by rhTM treatment. Gene set enrichment analysis revealed up-regulation of gene sets corresponding to cell proliferation/differentiation and anti-inflammation, such as the TGF-β pathway, and negative regulation of IL-6, upon rhTM treatment. Gene expression of heparan sulfate 6-O-sulfotransferase 1 and endothelial cell-specific molecule 1 (components of the endothelial glycocalyx) was significantly preserved by rhTM treatment, and their protein expression levels were maintained in endothelial cells. CONCLUSION AND IMPLICATIONS: Our findings show that rhTM treatment affected inflammation, cell proliferation/differentiation, and glycocalyx synthesis in serum and lung tissue, subsequently attenuating ARDS caused by endothelial injury.

Indexed as

GlycocalyxRespiratory Distress SyndromeAnimalsEndothelial CellsLipopolysaccharidesLungMaleMiceMice, Inbred C57BLThrombomodulinLipopolysaccharidesThrombomodulin

Identifiers

PMID32497259
PMCPMC7429482
OpenAlexW3033382871

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Registered trials

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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.