Evidence map›Paper›PMID 30775441›Full record

ArticleScience advances2019

Novel reprogramming of neutrophils modulates inflammation resolution during atherosclerosis.

Shuo Geng, Yao Zhang, Christina Lee, Liwu Li

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 78 citations in OpenAlex.

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  12. Neutrophils-biology and diversity.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Review
  13. Article
  14. Vesicular Messages from Dental Biofilms for Neutrophils.International journal of molecular sciences · 2024
    Article
  15. Neutrophils in Physiology and Pathology.Annual review of pathology · 2024
    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

4 authors at 1 institution in 1 country.

Shuo GengDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA 24061, USA.ORCID 0000-0001-9670-7294
Yao ZhangDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA 24061, USA.ORCID 0000-0002-0943-090X
Christina LeeDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA 24061, USA.ORCID 0000-0002-8607-4208
Liwu LiDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA 24061, USA.ORCID 0000-0001-8870-5299
Virginia Tech · US

Funding

Modulation of innate immune cellular homeostasis and inflammation resolutionR01HL115835 · NHLBI · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI LI, LIWU · 2012 to 2021
$3.6M
NHLBI NIH HHS R01 HL115835
6 · The paper itself

Abstract

Nonresolving inflammation perpetuated by innate leukocytes is involved in the pathogenesis of unstable atherosclerosis. However, the role and regulation of neutrophils related to nonresolving inflammation and atherosclerosis are poorly understood. We report herein that chronic subclinical endotoxemia, a risk factor for atherosclerosis, skewed neutrophils into a nonresolving inflammatory state with elevated levels of inflammatory mediators (Dectin-1, MMP9, and LTB4) and reduced levels of homeostatic mediators (LRRC32, TGFβ, and FPN). The polarization of neutrophils was due to ROS-mediated activation of oxCAMKII, caused by altered peroxisome homeostasis and reduced lysosome fusion. Application of 4-phenylbutyrate (4-PBA) enhanced peroxisome homeostasis of neutrophils, reduced oxCAMKII, and rebalanced the expression profiles of pro- and anti-inflammatory mediators. Adoptive transfer of neutrophils programmed by subclinical endotoxemia rendered exacerbated atherosclerosis. In contrast, transfer of ex vivo programmed neutrophils by 4-PBA reduced the pathogenesis of atherosclerosis. Our data define novel neutrophil dynamics associated with the progression and regression of atherosclerosis.

Indexed as

Cellular ReprogrammingDisease SusceptibilityAnimalsAtherosclerosisDisease Models, AnimalEndotoxemiaInflammationMaleMiceMice, KnockoutNeutrophilsPlaque, AtheroscleroticReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID30775441
PMCPMC6365109
OpenAlexW2911987051

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.