Evidence map›Paper›PMID 23322347›Full record

ReviewToxicological sciences : an official journal of the Society of Toxicology2013

Emerging mechanistic targets in lung injury induced by combustion-generated particles.

Marc W Fariss, M Ian Gilmour, Christopher A Reilly, Wolfgang Liedtke, Andrew J Ghio

Erratum issuedOpen access · bronzeAbstract readReview
In one paragraph

Review in Toxicological sciences : an official journal of the Society of Toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 9% 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, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. TRP Channels as Cellular Targets of Particulate Matter.International journal of molecular sciences · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Effect of collection methods on combustion particle physicochemical properties and their biological response in a human macrophage-like cell line.Journal of environmental science and health. Part A, Toxic/hazardous substances & environmental engineering · 2019
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

5 authors at 4 institutions in 2 countries.

Marc W FarissAltria Client Services Inc., Richmond, Virginia, USA.
M Ian Gilmour
Christopher A Reilly
Wolfgang Liedtke
Andrew J Ghio
Environmental Protection Agency · USAltria (United States) · USDuke University · USUniversity of Utah · US

Funding

TRP Channels and Air PollutionR01ES017431 · NIEHS · UNIVERSITY OF UTAH · PI REILLY, CHRISTOPHER A · 2009 to 2024
$5.3M
NIEHS NIH HHS R01 ES017431
6 · The paper itself

Abstract

The mechanism for biological effect following exposure to combustion-generated particles is incompletely defined. The identification of pathways regulating the acute toxicological effects of these particles provides specific targets for therapeutic manipulation in an attempt to impact disease following exposures. Transient receptor potential (TRP) cation channels were identified as "particle sensors" in that their activation was coupled with the initiation of protective responses limiting airway deposition and inflammatory responses, which promote degradation and clearance of the particles. TRPA1, V1, V4, and M8 have a capacity to mediate adverse effects after exposure to combustion-generated particulate matter (PM); relative contributions of each depend upon particle composition, dose, and deposition. Exposure of human bronchial epithelial cells to an organic extract of diesel exhaust particle was followed by TRPV4 mediating Ca(++) influx, increased RAS expression, mitogen-activated protein kinase signaling, and matrix metalloproteinase-1 activation. These novel pathways of biological effect can be targeted by compounds that specifically inhibit critical signaling reactions. In addition to TRPs and calcium biochemistry, humic-like substances (HLS) and cell/tissue iron equilibrium were identified as potential mechanistic targets in lung injury after particle exposure. In respiratory epithelial cells, iron sequestration by HLS in wood smoke particle (WSP) was associated with oxidant generation, cell signaling, transcription factor activation, and release of inflammatory mediators. Similar to WSP, cytotoxic insoluble nanosized spherical particles composed of HLS were isolated from cigarette smoke condensate. Therapies that promote bioelimination of HLS and prevent the disruption of iron homeostasis could function to reduce the harmful effects of combustion-generated PM exposure.

Indexed as

Air PollutantsCalciumCells, CulturedHumansIronLungMicroscopy, Electron, ScanningMicroscopy, Electron, TransmissionMitochondriaNicotianaParticle SizeSmokeTransient Receptor Potential ChannelsAir PollutantsCalciumIronSmokeTransient Receptor Potential Channels

Identifiers

PMID23322347
PMCPMC4447844
OpenAlexW2171504300

What OpenQuestion holds

Textmetadata
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.