Evidence map›Paper›PMID 27530451›Full record

ArticleScientific reports2016

DNMT1-PPARγ pathway in macrophages regulates chronic inflammation and atherosclerosis development in mice.

Jie Yu, Youzhu Qiu, Jie Yang, Shizhu Bian, Guozhu Chen, Mengyang Deng, Huali Kang, Lan Huang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

  1. Pooled it
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  8. How to measure and model cardiovascular aging.Cardiovascular research · 2025
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12 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Jie YuInstitute of Cardiovascular Diseases of the PLA , Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Youzhu QiuInstitute of Cardiovascular Diseases of the PLA , Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Jie YangInstitute of Cardiovascular Diseases of the PLA , Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Shizhu BianInstitute of Cardiovascular Diseases of the PLA , Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Guozhu ChenInstitute of Cardiovascular Diseases of the PLA , Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Mengyang DengInstitute of Cardiovascular Diseases of the PLA , Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Huali KangInstitute of Cardiovascular Diseases of the PLA , Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Lan HuangInstitute of Cardiovascular Diseases of the PLA , Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
Army Medical University · CNXinqiao Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DNA methyltransferase-mediated proinflammatory activation of macrophages is causally linked to the development of atherosclerosis (AS). However, the role of DNMT1, a DNA methylation maintenance enzyme, in macrophage polarization and AS development remains obscure. Here, we established transgenic mice with macrophage-specific overexpression of DNMT1 (Tg(DNMT1)) or PPAR-γ (Tg(PPAR-γ)) to investigate their effects on AS progression in ApoE-knockout mice fed an atherogenic diet. Primary macrophages were extracted to study the role of the DNMT1/PPAR-γ pathway in regulating inflammatory cytokine production. We demonstrated that Tg(DNMT1) significantly increased proinflammatory cytokine production in macrophages and plasma, and it accelerated the progression of AS in the atherogenic diet-treated ApoE-knockout mice. Further, we found that the DNA methylation status of the proximal PPAR-γ promoter was regulated by DNMT1 in macrophages. Notably, additional Tg(PPAR-γ) or pharmacological activation of PPAR-γ effectively prevented Tg(DNMT1)-induced proinflammatory cytokine production in macrophages and AS development in the mouse model. Finally, we demonstrated that elevated DNMT1 was correlated with decreased PPAR-γ, and increased proinflammatory cytokine production in the peripheral blood monocytes isolated from the patients with AS, compared to those of healthy donors. Our findings shed light on a novel strategy for the prevention and therapy of AS.

Indexed as

AnimalsApolipoproteins EAtherosclerosisCytokinesDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationHumansHypoglycemic AgentsInflammationMacrophage ActivationMacrophagesMaleMiceMice, Inbred C57BLMice, Knockout, ApoEPPAR gammaApolipoproteins ECytokinesDNA (Cytosine-5-)-Methyltransferase 1Dnmt1 protein, mouseHypoglycemic AgentsPPAR gammaRosiglitazoneThiazolidinediones

Identifiers

PMID27530451
PMCPMC4987643
OpenAlexW2514448694

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.