Evidence map›Paper›PMID 25330030›Full record

ArticlePloS one2014

HDAC6 deacetylase activity is critical for lipopolysaccharide-induced activation of macrophages.

Bing Yan, Songbo Xie, Zhu Liu, Jie Ran, Yuanyuan Li, Jian Wang, Yang Yang, Jun Zhou, Dengwen Li, Min Liu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Targeting HDAC6 improves anti-CD47 immunotherapy.Journal of experimental & clinical cancer research : CR · 2024
    Article
  3. Article
  4. Review
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  6. Review
  7. OGT suppresses S6K1-mediated macrophage inflammation and metabolic disturbance.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  8. Review
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  12. Review
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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

10 authors at 2 institutions in 1 country.

Bing YanState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Songbo XieState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Zhu LiuKey Laboratory of Immune Microenvironment and Disease of the Ministry of Education, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Jie RanState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Yuanyuan LiState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Jian WangState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Yang YangState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Jun ZhouState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Dengwen LiState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China.
Min LiuKey Laboratory of Immune Microenvironment and Disease of the Ministry of Education, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Nankai University · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activated macrophages play an important role in both innate and adaptive immune responses, and aberrant activation of macrophages often leads to inflammatory and immune disorders. However, the molecular mechanisms of how macrophages are activated are not fully understood. In this study, we identify a novel role for histone deacetylse 6 (HDAC6) in lipopolysaccharide (LPS)-induced macrophage activation. Our data show that suppression of HDAC6 activity significantly restrains LPS-induced activation of macrophages and production of pro-inflammatory cytokines. Further study reveals that the regulation of macrophage activation by HDAC6 is independent of F-actin polymerization and filopodium formation; instead, it is mediated by the effects of HDAC6 on cell adhesion and microtubule acetylation. These data thus suggest that HDAC6 is an important regulator of LPS-induced macrophage activation and might be a potential target for the management of inflammatory disorders.

Indexed as

Immunity, InnateAcetylationActinsAnimalsCell AdhesionCytokinesHistone Deacetylase 6Histone Deacetylase InhibitorsHistone DeacetylasesInflammationLipopolysaccharidesMacrophage ActivationMacrophagesMiceMicrotubulesPseudopodiaActinsCytokinesHdac6 protein, mouseHistone Deacetylase 6Histone Deacetylase InhibitorsHistone DeacetylasesLipopolysaccharides

Identifiers

PMID25330030
PMCPMC4199742
OpenAlexW1970211961

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.