Evidence map›Paper›PMID 25860573›Full record

ArticlePloS one2015

TLR4/NF-κB signaling contributes to chronic unpredictable mild stress-induced atherosclerosis in ApoE-/- mice.

Ya Ling Tang, Jian Hong Jiang, Shuang Wang, Zhu Liu, Xiao Qing Tang, Juan Peng, Yong-Zong Yang, Hong-Feng Gu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

30 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Research progress of stem cells in the treatment of atherosclerosis.Frontiers in cell and developmental biology · 2025
    Review
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  7. Review
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  13. Review
  14. The structure, biosynthesis, and biological roles of fetuin-A: A review.Frontiers in cell and developmental biology · 2022
    Review
  15. Review
  16. Recent Progress of Chronic Stress in the Development of Atherosclerosis.Oxidative medicine and cellular longevity · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. Article
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 1 institution in 1 country.

Ya Ling TangKey Lab for Arteriosclerology of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, People's Republic of China.
Jian Hong JiangChuanshan College, University of South China, Hengyang, 421001, People's Republic of China.
Shuang WangKey Lab for Arteriosclerology of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, People's Republic of China.
Zhu LiuChuanshan College, University of South China, Hengyang, 421001, People's Republic of China.
Xiao Qing TangDepartment of Physiology & Institute of Neuroscience, University of South China, Hengyang, 421001, People's Republic of China.
Juan PengKey Lab for Arteriosclerology of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, People's Republic of China.
Yong-Zong YangKey Lab for Arteriosclerology of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, People's Republic of China.
Hong-Feng GuKey Lab for Arteriosclerology of Hunan Province, Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, People's Republic of China; Department of Physiology & Institute of Neuroscience, University of South China, Hengyang, 421001, People's Republic of China.
University of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveChronic stress is an important risk factor for atherosclerotic diseases. Our previous studies have shown that chronic unpredictable mild stress (CUMS) accelerates atherosclerosis and up-regulates TLR4/NF-κB expression in apoE-/- mice. However, TLR4/NF-κB signaling whether directly contributes to the development of atherosclerosis in CUMS mice is unclear. We hypothesized that the interference of TLR4/NF-κB can ameliorate CUMS-induced inflammation and atherosclerosis in apoE-/- mice.

methodsApoE-/- mice were exposed to 12 weeks CUMS. Ad-siRNA TLR4 was given by tail vein injection (10 μl/mouse, every 5 days), and PDTC (an inhibitor of NF-κB) was given by intraperitoneal injection (60 mg/kg, once a day). Plasma corticosterone concentrations were determined by solid-phase 125I radioimmunoassay. Atherosclerosis lesions in aortic sinuses were evaluated and quantified by IMAGEPRO PLUS. Western blotting was used to detect the expression of TLR4, NF-κB, and IL-1β in aortas of the mice. Plasma lipid profiles, IL-1β, TNF-α, and MCP-1 were measured by ELISA.

resultsOur results indicated that CUMS apoE-/- mice treatment with siRNA TLR4 significantly decreased atherosclerosis and down-regulated TLR4, NF-κB, and inflammatory cytokines. PDTC also remarkably reduced atherosclerosis and the levels of IL-1β, TNF-α and MCP-1 in plasma. However, Treatment with siRNA TLR4 or PDTC had no effect on plasma corticosterone levels, and lipid profiles.

conclusionsTLR4/NF-κB pathway may participate in CUMS-induced atherosclerosis through activation of proinflammatory cytokines in apoE-/- mice. Our data may provide a new potential therapeutic target for prevention of CUMS -induced atherosclerosis.

Indexed as

Signal TransductionStress, PhysiologicalAnimalsAortaApolipoproteins EAtherosclerosisCorticosteroneCytokinesDisease Models, AnimalInflammation MediatorsLipidsMaleMiceMice, KnockoutNF-kappa BProlineApolipoproteins ECorticosteroneCytokinesInflammation MediatorsLipidsNF-kappa BProlineprolinedithiocarbamateRNA, Small InterferingThiocarbamatesToll-Like Receptor 4

Identifiers

PMID25860573
PMCPMC4393302
OpenAlexW2075211583

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.