Evidence map›Paper›PMID 40715151›Full record

ArticleScientific reports2025

Vasoprotective effects of lysophosphatidic acid inhibit vascular injury caused by SARS-CoV-2 infection.

Fumitaka Muramatsu, Naoi Hosoe, Tatsuya Suzuki, Teppei Shimamura, Yumiko Hayashi, Kazuhiro Takara, Lamri Lynda, Anna Shimizu, Weizhen Jia, Yoshimi Noda and 3 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

13 authors.

Fumitaka MuramatsuDepartment of Signal Transduction, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan.
Naoi HosoeDepartment of Integrative Vascular Biology, Faculty of Medical Sciences, University of Fukui, 23- 3 Matsuoka-Shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan.
Tatsuya SuzukiDepartment of Microbiology, Juntendo University School of Medicine, Tokyo, 113- 8421, Japan.
Teppei ShimamuraDepartment of Computational and Systems Biology, Medical Research Institute, Institute of Science Tokyo, Bunkyo-ku, Tokyo, 113-8510, Japan.
Yumiko HayashiDepartment of Integrative Vascular Biology, Faculty of Medical Sciences, University of Fukui, 23- 3 Matsuoka-Shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan.
Kazuhiro TakaraDepartment of Integrative Vascular Biology, Faculty of Medical Sciences, University of Fukui, 23- 3 Matsuoka-Shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan.
Lamri LyndaDepartment of Integrative Vascular Biology, Faculty of Medical Sciences, University of Fukui, 23- 3 Matsuoka-Shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan.
Anna ShimizuDepartment of Integrative Vascular Biology, Faculty of Medical Sciences, University of Fukui, 23- 3 Matsuoka-Shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan.
Weizhen JiaDepartment of Signal Transduction, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan.
Yoshimi NodaDepartment of Signal Transduction, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan.
Nobuyuki TakakuraDepartment of Signal Transduction, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan.
Toru OkamotoDepartment of Microbiology, Juntendo University School of Medicine, Tokyo, 113- 8421, Japan.
Hiroyasu KidoyaDepartment of Integrative Vascular Biology, Faculty of Medical Sciences, University of Fukui, 23- 3 Matsuoka-Shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan. kidoya@u-fukui.ac.jp.

Funding

Japan Agency for Medical Research and Development 20fk0108303h0001JSPS Grant-in-Aid for Challenging Research (Exploratory) 22K19453JSPS Grant-in-Aid for Transformative Research Areas (A) 23H04931JST FOREST Program JPMJFR2160PRESTO-JST JPMJPR1944
6 · The paper itself

Abstract

Vasculitis and vascular injury are induced in coronavirus disease 2019 (COVID-19) patients, suggesting an association between multi-organ failure and sequelae. Vascular endothelial dysfunction induced by severe acute respiratory syndrome-related coronavirus-2 (SARS-CoV-2) disrupts vascular barrier function, activates coagulation pathways, and induces extravasation of inflammatory cells. In addition to employing standard anti-inflammatory and antiviral agents, using treatments that stabilize and protect blood vessels following SARS-CoV-2 infection is a potentially effective strategy to relieve COVID-19 severity. Here, we focused on the vasoprotective effects of lysophosphatidic acid (LPA), a lipid mediator with diverse activities, and investigated whether it could be a novel therapeutic for COVID-19. Three-dimensional cultures of various human vascular endothelial cells that form luminal structures showed increased expression of LPA4 and entry receptors for SARS-CoV-2 infection, mimicking blood vessels in vivo. Validation using this culture system showed that LPA attenuated SARS-CoV-2 infection-induced vascular destruction and the activation of inflammatory signaling. In experiments with infected animals, LPA administration protected blood vessels and suppressed inflammation and vascular damage in lung tissue. The activation of LPA signaling in vascular endothelial cells may be an effective therapeutic approach for mitigating vascular injury in COVID-19.

Indexed as

COVID-19COVID-19 Drug TreatmentLysophospholipidsSARS-CoV-2Vascular System InjuriesAnimalsEndothelial CellsHumansMaleMiceSignal Transductionlysophosphatidic acidLysophospholipidsCOVID-19Lysophosphatidic acid (LPA)SARS-CoV-2Vascular endothelial cellVascular injury

Identifiers

PMID40715151
PMCPMC12297521

What OpenQuestion holds

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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.