Evidence map›Paper›PMID 37432325›Full record

ArticleNutrients2023

Docosahexaenoic Acid Alleviates Trimethylamine-

Jia-Ning Syu, Hung-Yu Lin, Tun Yu Huang, Der-Yen Lee, En-Pei Isabel Chiang, Feng-Yao Tang

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. 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

6 authors at 3 institutions in 1 country.

Jia-Ning SyuBiomedical Science Laboratory, Department of Nutrition, China Medical University, Taichung 40604, Taiwan.ORCID 0000-0001-9991-3835
Hung-Yu LinResearch Assistant Center, Show Chwan Memorial Hospital, Changhua 500, Taiwan.ORCID 0000-0002-9035-5408
Tun Yu HuangProspective Wound Medicine Research Center, Show Chwan Memorial Hospital, Changhua 500, Taiwan.
Der-Yen LeeGraduate Institute of Integrated Medicine, China Medical University, Taichung 40604, Taiwan.
En-Pei Isabel ChiangDepartment of Food Science and Biotechnology, National Chung Hsing University, Taichung 402, Taiwan.ORCID 0000-0002-0158-0962
Feng-Yao TangBiomedical Science Laboratory, Department of Nutrition, China Medical University, Taichung 40604, Taiwan.
China Medical University · TWChang Bing Show Chwan Memorial Hospital · TWNational Chung Hsing University · TW

Funding

China Medical University CMU110-MF-62, CMU111-MF-70National Science and Technology Council (NSTC), Taiwan 107-2320-B-039-008-MY3, 107-2320-B-005-003 -MY3, 107-2621-M-005-008 -MY3, 107-2321-B-005-009, 108-2321-B-005-004, 110-2320-B-039-049-MY3, 110-2320-B-005-008-MY3, 110-2320-B-005-003-MY3, 111-2811-B-039-003, 111-2811-B-039-019Show Chwan Memorial Hospital SRD-110031, SRD-110032
6 · The paper itself

Abstract

backgroundHuman endothelial progenitor cells (hEPCs), originating from hemangioblasts in bone marrow (BM), migrate into the blood circulation, differentiate into endothelial cells, and could act as an alternative tool for tissue regeneration. In addition, trimethylamine-

resultsOur results demonstrated that TMAO dose-dependently impaired human stem cell factor (SCF)-mediated neovascularization in hEPCs. The action of TMAO was through the inactivation of Akt/endothelial nitric oxide synthase (eNOS), MAPK/ERK signaling pathways, and an upregulation of microRNA (miR)-221. Docosahexaenoic acid (DHA) could effectively inhibit the cellular miR-221 level and induce the phosphorylation level of Akt/eNOS, MAPK/ERK signaling molecules, and neovascularization in hEPCs. DHA enhanced cellular amounts of reduced form glutathione (GSH) through an increased expression of the gamma-glutamylcysteine synthetase (γ-GCS) protein.

conclusionsTMAO could significantly inhibit SCF-mediated neovascularization, in part in association with an upregulation of miR-221 level, inactivation of Akt/eNOS and MAPK/ERK cascades, suppression of γ-GCS protein, and decreased levels of GSH and GSH/GSSG ratio. Furthermore, the DHA could alleviate the detrimental effects of TMAO and induce neovasculogenesis through suppression of miR-221 level, activation of Akt/eNOS and MAPK/ERK signaling cascades, increased expression of γ-GCS protein, and increment of cellular GSH level and GSH/GSSG ratio in hEPCs.

Indexed as

Endothelial Progenitor CellsMicroRNAsDocosahexaenoic AcidsGlutathione DisulfideHumansMethylaminesNeovascularization, PathologicOxidesProto-Oncogene Proteins c-aktDocosahexaenoic AcidsGlutathione DisulfideMethylaminesMicroRNAsOxidesProto-Oncogene Proteins c-akttrimethylaminetrimethyloxaminedocosahexaenoic acidendothelial nitric oxide synthaseendothelial progenitor cellsglutathionemicroRNA 221trimethylamine-N-oxide

Identifiers

PMID37432325
PMCPMC10180856
OpenAlexW4381939653

What OpenQuestion holds

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LicenceCC BY
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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.