Evidence map›Paper›PMID 26108756›Full record

ArticleParticle and fibre toxicology2015

Exposure to concentrated ambient particulate matter induces reversible increase of heart weight in spontaneously hypertensive rats.

Zhekang Ying, Xiaoyun Xie, Yuntao Bai, Minjie Chen, Xiaoke Wang, Xuan Zhang, Masako Morishita, Qinghua Sun, Sanjay Rajagopalan

Open access · goldAbstract read
In one paragraph

Article in Particle and fibre toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.7field-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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Association between PMFrontiers in public health · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Air Pollution: Another Threat to HDL Function.International journal of molecular sciences · 2022
    Review
  10. Deficiency of interleukin-6 receptor ameliorates PMEcotoxicology and environmental safety · 2022
    Article
  11. Review
  12. Impacts of Environmental Insults on Cardiovascular Aging.Current environmental health reports · 2022
    Review
  13. Environmental health perspectives · 2021
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

9 authors at 4 institutions in 2 countries.

Zhekang YingDepartment of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai, 200120, People's Republic of China. zying@medicine.umaryland.edu.
Xiaoyun XieDivision of Geriatric Medicine, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, People's Republic of China. xiaoyunxietj@126.com.
Yuntao BaiDivision of Environmental Health Sciences, College of Public Health, The Ohio State University, Columbus, OH, USA. yuntao.bai@osumc.edu.
Minjie ChenDepartment of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai, 200120, People's Republic of China. chen_minjie@hotmail.com.
Xiaoke WangDepartment of Medicine Cardiology Division, University of Maryland School of Medicine, 20 Penn Street, Baltimore, MD, 21201, USA. xwang2@medicine.umaryland.edu.
Xuan ZhangDepartment of Medicine Cardiology Division, University of Maryland School of Medicine, 20 Penn Street, Baltimore, MD, 21201, USA. xzhang1@medicine.umaryland.edu.
Masako MorishitaDepartment of Environmental Health Sciences, University of Michigan, Ann Arbor, MI, USA. tomoko@umich.edu.
Qinghua SunDivision of Environmental Health Sciences, College of Public Health, The Ohio State University, Columbus, OH, USA. qsun@cph.osu.edu.
Sanjay RajagopalanDepartment of Medicine Cardiology Division, University of Maryland School of Medicine, 20 Penn Street, Baltimore, MD, 21201, USA. srajagopalan@medicine.umaryland.edu.
University of Maryland, Baltimore · USThe Ohio State University · USTongji University · CNUniversity of Michigan–Ann Arbor · US

Funding

Air Pollution and Hypertension: Vascular MechanismsR01ES015146 · NIEHS · UNIVERSITY OF MARYLAND BALTIMORE · PI RAJAGOPALAN, SANJAY · 2007 to 2018
$4.5M
Environmental Triggers of Cardiometabolic DiseaseR01ES019616 · NIEHS · UNIVERSITY OF MARYLAND BALTIMORE · PI BROOK, ROBERT DANIEL, RAJAGOPALAN, SANJAY · 2011 to 2020
$3.0M
Diet-Environment Interactions in InflammationR01ES017290 · NIEHS · UNIVERSITY OF MARYLAND BALTIMORE · PI RAJAGOPALAN, SANJAY · 2010 to 2014
$1.8M
Hypothalamic Inflammation and PM2.5 Exposure-Induced Insulin ResistanceR01ES024516 · NIEHS · UNIVERSITY OF MARYLAND BALTIMORE · PI YING, ZHEKANG · 2014 to 2018
$1.5M
Air Pollution Exposure/Atherosclerosis:Vascular MechanismR01ES013406 · NIEHS · OHIO STATE UNIVERSITY · PI RAJAGOPALAN, SANJAY · 2004 to 2007
$1.3M
NIEHS NIH HHS R01 ES013406NIEHS NIH HHS R01ES013406NIEHS NIH HHS R01 ES015146NIEHS NIH HHS R01ES015146NIEHS NIH HHS R01 ES017290NIEHS NIH HHS R01 ES019616NIEHS NIH HHS R01 ES024516NIEHS NIH HHS R01ES024516
6 · The paper itself

Abstract

backgroundExposure to ambient PM2.5 increases cardiovascular mortality and morbidity. To delineate the underlying biological mechanism, we investigated the time dependence of cardiovascular response to chronic exposure to concentrated ambient PM2.5 (CAP).

methodsSpontaneously hypertensive rats (SHR) were exposed to CAP for 15 weeks, and blood pressure (BP), cardiac function and structure, and inflammations of lung, hypothalamus, and heart were measured at different time points.

resultsChronic exposure to CAP significantly increased BP, and withdrawal from CAP exposure restored BP. Consistent with its BP effect, chronic exposure to CAP significantly decreased cardiac stroke volume and output in SHR, accompanied by increased heart weight and increased cardiac expression of hypertrophic markers ACTA1 and MYH7. Withdrawal from CAP exposure restored cardiac function, weight, and expression of hypertrophic markers, supporting the notion that cardiac dysfunction and hypertrophy is subsequent to hypertension. In agreement with the role of systemic inflammation in mediating the cardiovascular effects of CAP exposure, chronic exposure to CAP markedly increased expression of pro-inflammatory cytokines in lung, heart, and hypothalamus. However, withdrawal from exposure resolves inflammation in the heart and hypothalamus, but not in the lung, suggesting that CAP exposure-induced systemic inflammation may be independent of pulmonary inflammation.

conclusionChronic exposure to CAP induces reversible cardiac dysfunction and hypertrophy, which is likely to be subsequent to the elevation in BP and induction of systemic inflammation as evidenced by increased mRNA expression of pro-inflammatory cytokines in diverse tissues.

Indexed as

ActinsAnimalsBlood PressureDisease Models, AnimalHypertensionHypertrophy, Left VentricularHypothalamusInflammation MediatorsLungMaleMyocardiumMyosin Heavy ChainsParticulate MatterPneumoniaRats, Inbred SHRStroke VolumeActinsInflammation MediatorsMYH7 protein, ratMyosin Heavy ChainsParticulate Matter

Identifiers

PMID26108756
PMCPMC4479240
OpenAlexW1932718020

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.