Evidence map›Paper›PMID 24981836›Full record

ArticleCell metabolism2014

Lysophospholipid acyltransferases mediate phosphatidylcholine diversification to achieve the physical properties required in vivo.

Takeshi Harayama, Miki Eto, Hideo Shindou, Yoshihiro Kita, Eiji Otsubo, Daisuke Hishikawa, Satoshi Ishii, Kenji Sakimura, Masayoshi Mishina, Takao Shimizu

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 185 citations in OpenAlex.

  1. Pooled it
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  7. Ferroptosis: The Demise of Cells Through Phospholipid Peroxidation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 6 institutions in 1 country.

Takeshi HarayamaDepartment of Lipid Signaling, Research Institute, National Center for Global Health and Medicine, Shinjuku, Tokyo 162-8655, Japan.
Miki EtoDepartment of Lipid Signaling, Research Institute, National Center for Global Health and Medicine, Shinjuku, Tokyo 162-8655, Japan; Department of Lipidomics, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.
Hideo ShindouDepartment of Lipid Signaling, Research Institute, National Center for Global Health and Medicine, Shinjuku, Tokyo 162-8655, Japan.
Yoshihiro KitaDepartment of Lipidomics, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.
Eiji OtsuboDepartment of Lipid Signaling, Research Institute, National Center for Global Health and Medicine, Shinjuku, Tokyo 162-8655, Japan; Advanced Medical Research Department, Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Kanagawa 227-0033, Japan.
Daisuke HishikawaDepartment of Lipid Signaling, Research Institute, National Center for Global Health and Medicine, Shinjuku, Tokyo 162-8655, Japan.
Satoshi IshiiDepartment of Immunology, Graduate School of Medicine, Akita University, Akita 010-8543, Japan.
Kenji SakimuraDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata 951-8585, Japan.
Masayoshi MishinaBrain Science Laboratory, The Research Organization of Science and Technology, Ritsumeikan University, Kusatsu, Shiga 525-8577, Japan.
Takao ShimizuDepartment of Lipid Signaling, Research Institute, National Center for Global Health and Medicine, Shinjuku, Tokyo 162-8655, Japan; Department of Lipidomics, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan. Electronic address: tshimizu@ri.ncgm.go.jp.
National Center for Global Health and Medicine · JPAkita University · JPMitsubishi Chemical (Japan) · JPNiigata University · JPRitsumeikan University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The acyl-chain composition of the major mammalian phospholipid phosphatidylcholine (PC) is distinct in various tissues. Although it was classically suggested that PC diversity is acquired through acyl-chain remodeling, the mechanisms and biological relevance of acyl-chain diversity remain unclear. Here, we show that differences in the substrate selectivity of lysophospholipid acyltransferases regulate tissue PC acyl-chain composition through contribution of both the de novo and remodeling pathways, depending on the fatty acid species. Unexpectedly, while dipalmitoyl-PC (DPPC) is enriched through the remodeling pathway, several polyunsaturated PC molecules accumulate during the de novo pathway. We confirmed this concept for DPPC in pulmonary surfactant and showed that the biophysical properties of this lipid are important to prevent the early onset of acute lung injury. We propose a model of harmonized processes for phospholipid diversification to satisfy in vivo requirements, with an example of its biological relevance.

Indexed as

1,2-Dipalmitoylphosphatidylcholine1-Acylglycerophosphocholine O-AcyltransferaseAnimalsChemokinesCHO CellsCricetinaeCricetulusCytokinesLung InjuryMiceMice, Inbred C57BLPhosphatidylcholinesSurface-Active Agents1,2-Dipalmitoylphosphatidylcholine1-Acylglycerophosphocholine O-Acyltransferase1-palmitoyl-2-oleoylphosphatidylcholineChemokinesCytokinesPhosphatidylcholinesSurface-Active Agents

Identifiers

PMID24981836
OpenAlexW2029958712

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.