Evidence map›Paper›PMID 26148452›Full record

ReviewCardiovascular toxicology2016

Air Pollution-Induced Vascular Dysfunction: Potential Role of Endothelin-1 (ET-1) System.

Jordan Finch, Daniel J Conklin

Open access · greenAbstract readReview
In one paragraph

Review in Cardiovascular toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.7field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 75 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Open veterinary journal · 2023
    Article
  12. Article
  13. Article
  14. Environmental Pollution and Peripheral Artery Disease.Risk management and healthcare policy · 2021
    Review
  15. Prevention of Fine Dust-Induced Vascular Senescence byAntioxidants (Basel, Switzerland) · 2020
    Article
  16. Inflammatory effects of particulate matter air pollution.Environmental science and pollution research international · 2020
    Review
  17. AqueousJournal of diabetes and metabolic disorders · 2020
    Article
  18. Article
  19. Cardiovascular adaptations to particle inhalation exposure: molecular mechanisms of the toxicology.American journal of physiology. Heart and circulatory physiology · 2020
    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

2 authors at 2 institutions in 1 country.

Jordan FinchDepartment of Pharmacology and Toxicology, School of Medicine, University of Louisville, 580 S. Preston Street, Louisville, KY, 40202, USA.
Daniel J ConklinDivision of Cardiovascular Medicine, Department of Medicine, Diabetes and Obesity Center, University of Louisville, 580 S. Preston Street, Delia Baxter Building, Rm 404E, Louisville, KY, 40202, USA. dj.conklin@louisville.edu.
University of Louisville · USUniversity of Louisville Hospital · US

Funding

Project 5 - Metabolomic Analysis of AtherothrombosisP20GM103492 · NIGMS · UNIVERSITY OF LOUISVILLE · PI BHATNAGAR, ARUNI · 2012 to 2017
$13.8M
UOFL ENVIRONMENTAL HEALTH SCIENCES TRAINING PROGRAMT32ES011564 · NIEHS · UNIVERSITY OF LOUISVILLE · PI David W Hein, John Pierce Wise · 2004 to 2026
$7.1M
Endothelial Progenitor Cells and Particulate Air PollutionR01ES019217 · NIEHS · UNIVERSITY OF LOUISVILLE · PI BHATNAGAR, ARUNI, O'TOOLE, TIMOTHY E · 2011 to 2022
$6.0M
Cardioprotective Mechanisms of Glutathione S-transferase PR01HL089380 · NHLBI · UNIVERSITY OF LOUISVILLE · PI CONKLIN, DANIEL JOSEPH · 2008 to 2012
$2.1M
NHLBI NIH HHS R01 HL089380NIEHS NIH HHS R01 ES019217NIEHS NIH HHS T32 ES011564NIGMS NIH HHS P20 GM103492
6 · The paper itself

Abstract

Exposure to air pollution negatively impacts cardiovascular health. Studies show that increased exposure to a number of airborne pollutants increases the risk for cardiovascular disease progression, myocardial events, and cardiovascular mortality. A hypothesized mechanism linking air pollution and cardiovascular disease is the development of systemic inflammation and endothelium dysfunction, the latter of which can result from an imbalance of vasoactive factors within the vasculature. Endothelin-1 (ET-1) is a potent peptide vasoconstrictor that plays a significant role in regulating vascular homeostasis. It has been reported that the production and function of ET-1 and its receptors are upregulated in a number of disease states associated with endothelium dysfunction including hypertension and atherosclerosis. This mini-review surveys epidemiological and experimental air pollution studies focused on ET-1 dysregulation as a plausible mechanism underlying the development of cardiovascular disease. Although alterations in ET-1 system components are observed in some studies, there remains a need for future research to clarify whether these specific changes are compensatory or causally related to vascular injury and dysfunction. Moreover, further research may test the efficacy of selective ET-1 pharmacological interventions (e.g., ETA receptor inhibitors) to determine whether these treatments could impede the deleterious impact of air pollution exposure on cardiovascular health.

Indexed as

Air PollutantsAir PollutionAnimalsCardiovascular DiseasesEndothelin-1Endothelium, VascularEnvironmental ExposureHumansOccupational ExposurePrognosisReceptors, EndothelinRisk AssessmentRisk FactorsSignal TransductionTobacco Smoke PollutionAir PollutantsEndothelin-1Receptors, EndothelinTobacco Smoke PollutionAir pollutionCardiovascular diseaseEndothelin-1Endothelium dysfunctionET-1Vascular dysfunctionVasoconstriction

Identifiers

PMID26148452
PMCPMC4704997
OpenAlexW792142886

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.