Evidence map›Paper›PMID 36369824›Full record

ArticleAnnals of medicine2022

Decrease in serum levels of autotaxin in COVID-19 patients.

Takuya Shimura, Makoto Kurano, Koh Okamoto, Daisuke Jubishi, Hideki Hashimoto, Kuniyuki Kano, Koji Igarashi, Satoshi Shimamoto, Junken Aoki, Kyoji Moriya and 1 more

Open access · goldAbstract read
In one paragraph

Article in Annals of medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.3field-weighted citation impact, top 47% 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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

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 3 institutions in 1 country.

Takuya ShimuraDepartment of Clinical Laboratory, The University of Tokyo Hospital, Tokyo, Japan.
Makoto KuranoDepartment of Clinical Laboratory, The University of Tokyo Hospital, Tokyo, Japan.
Koh OkamotoDepartment of Infectious Diseases, The University of Tokyo Hospital, Tokyo, Japan.
Daisuke JubishiDepartment of Infectious Diseases, The University of Tokyo Hospital, Tokyo, Japan.
Hideki HashimotoDepartment of Infectious Diseases, The University of Tokyo Hospital, Tokyo, Japan.
Kuniyuki KanoDepartment of Health Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Koji IgarashiBioscience Division, TOSOH Corporation, Kanagawa, Japan.
Satoshi ShimamotoBioscience Division, TOSOH Corporation, Kanagawa, Japan.
Junken AokiDepartment of Health Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Kyoji MoriyaDepartment of Infectious Diseases, The University of Tokyo Hospital, Tokyo, Japan.
Yutaka YatomiDepartment of Clinical Laboratory, The University of Tokyo Hospital, Tokyo, Japan.
University of Tokyo Hospital · JPThe University of Tokyo · JPTosoh (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIn order to identify therapeutic targets in Coronavirus disease 2019 (COVID-19), it is important to identify molecules involved in the biological responses that are modulated in COVID-19. Lysophosphatidic acids (LPAs) are involved in the pulmonary inflammation and fibrosis are one of the candidate molecules. The aim of this study was to evaluate the association between the serum levels of autotaxin (ATX), which are enzymes involved in the synthesis of lysophosphatidic acids. MATERIAL AND

methodsWe enrolled 134 subjects with COVID-19 and 58 normal healthy subjects for the study. We measured serum ATX levels longitudinally in COVID-19 patients and investigated the time course and the association with severity and clinical parameters.

resultsThe serum ATX levels were reduced in all patients with COVID-19, irrespective of the disease severity, and were negatively associated with the serum CRP, D-dimer, and anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antibody levels. DISCUSSION: Considering the biological properties of LPAs in the pulmonary inflammation and fibrosis, modulation of ATX might be compensatory biological responses to suppress immunological overreaction especially in the lung, which is an important underlying mechanism for the mortality of the disease.

conclusionsCOVID-19 patients showed a decrease in the serum levels of ATX, irrespective of the disease severity. Key MessagesAutotaxin (ATX) is an enzyme involved in the synthesis of lysophosphatidic acid (LPA), which has been reported to be involved in pulmonary inflammation and fibrosis. Patients with COVID-19 show decrease in the serum levels of ATX. Modulation of ATX might be compensatory biological responses to suppress immunological overreaction.

Indexed as

COVID-19Phosphoric Diester HydrolasesFibrosisHumansLungLysophospholipase DLysophospholipidsSARS-CoV-2Lysophospholipase DLysophospholipidsPhosphoric Diester HydrolasesAutotaxinCOVID-19inflammationlysophosphatidic acidsseverity

Identifiers

PMID36369824
PMCPMC9665086
OpenAlexW4309074159

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.