Evidence map›Paper›PMID 36536251›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023

Apolipoprotein D modulates lipid mediators and osteopontin in an anti-inflammatory direction.

Makoto Kurano, Kazuhisa Tsukamoto, Shigeo Kamitsuji, Naoyuki Kamatani, Koji Hasegawa, Masumi Hara, Toshio Ishikawa, Yutaka Yatomi, Tamio Teramoto

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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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  12. Review
  13. Apolipoprotein D in Oxidative Stress and Inflammation.Antioxidants (Basel, Switzerland) · 2023
    Review
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 4 institutions in 1 country.

Makoto KuranoDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kazuhisa TsukamotoDepartment of Internal Medicine, Teikyo University School of Medicine, 2-11-1, Kaga, Itabashi-Ku, Tokyo, 173-8605, Japan. kazuhisatky@med.teikyo-u.ac.jp.
Shigeo KamitsujiStaGen Co., Ltd., Statistical Genetics Analysis Division, Tokyo, Japan.
Naoyuki KamataniStaGen Co., Ltd., Statistical Genetics Analysis Division, Tokyo, Japan.
Koji HasegawaDepartment of Metabolism, Diabetes and Nephrology, Aizu Medical Center, Fukushima Medical University, Fukushima, Japan.
Masumi HaraDepartment of Medicine IV, Mizonokuchi Hospital, Teikyo University School of Medicine, Kawasaki, Japan.
Toshio IshikawaDepartment of Internal Medicine, Teikyo University School of Medicine, 2-11-1, Kaga, Itabashi-Ku, Tokyo, 173-8605, Japan.
Yutaka YatomiDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Tamio TeramotoDepartment of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.
Teikyo University · JPStaGen (Japan) · JPThe University of Tokyo · JPFukushima Medical University · JP

Funding

Japan Agency for Medical Research and Development LEAPJapan Society for the Promotion of Science 16H06236Japan Society for the Promotion of Science 16K15330
6 · The paper itself

Abstract

backgroundHDL has been proposed to possess anti-inflammatory properties; however, the detail mechanisms have not been fully elucidated.

methodsWe investigated the roles of Apolipoprotein D (ApoD) in the pathogenesis of inflammation in the mouse model of diet-induced obesity and that of lipopolysaccharide-induced sepsis and the in vitro experiments. Furthermore, we analyzed serum ApoD levels in human subjects.

resultsThe overexpression of human ApoD decreased the plasma IL-6 and TNF-a levels in both mice models. Lipidomics analyses demonstrated association of ApoD with increase of arachidonic acid, eicosapentaenoic acid, and docosahexaenoic acid, as well as of their metabolites, and of the anti-inflammatory molecule sphingosine 1-phosphate, and decrease of proinflammatory lysophosphatidic acids and lysophosphatidylinositol. ApoD-containing lipoproteins might directly bind eicosapentaenoic acid and docosahexaenoic acid. The modulations of the lysophosphatidic acid and sphingosine 1-phosphate levels resulted from the suppression of autotaxin expression and elevation of apolipoprotein M (ApoM), respectively. Moreover, ApoD negatively regulated osteopontin, a proinflammatory adipokine. The activation of PPARg by ApoD might suppress autotaxin and osteopontin. Serum ApoD levels were negatively correlated with the serum osteopontin and autotaxin levels and, positively with serum ApoM levels.

conclusionApoD is an anti-inflammatory apolipoprotein, which modulates lipid mediators and osteopontin in an anti-inflammatory direction.

Indexed as

Eicosapentaenoic AcidOsteopontinAnimalsAnti-Inflammatory AgentsApolipoproteins DDocosahexaenoic AcidsEicosanoidsHumansLysophospholipidsMiceSphingosineAnti-Inflammatory AgentsApolipoproteins DDocosahexaenoic AcidsEicosanoidsEicosapentaenoic AcidLysophospholipidsOsteopontinSphingosinesphingosine 1-phosphateApolipoprotein DApolipoprotein MAutotaxinEicosanoidsHDLInflammationInsulin resistanceLysophospholipidsOsteopontinw3-fatty acids

Identifiers

PMID36536251
OpenAlexW4311914381

What OpenQuestion holds

Textmetadata
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.