Evidence map›Paper›PMID 18226603›Full record

ReviewFree radical biology & medicine2008

Silica binding and toxicity in alveolar macrophages.

Raymond F Hamilton, Sheetal A Thakur, Andrij Holian

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 2% 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

162 citing papers in PubMed, 1 synthesis or guideline pooled it, 409 citations in OpenAlex.

  1. Guideline
  2. Article
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  11. Pulmonary injury following exposure to amorphous silicon dioxide nanoparticles inExperimental biology and medicine (Maywood, N.J.) · 2026
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Silicosis: from pathogenesis to therapeutics.Frontiers in pharmacology · 2025
    Review
  18. Article
  19. Article
  20. Article

102 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

3 authors at 2 institutions in 1 country.

Raymond F HamiltonDepartment of Biomedical and Pharmaceutical Sciences, Center for Environmental Health Sciences, University of Montana, 32 Campus Drive, SB 154, Missoula, MT 59812, USA.
Sheetal A Thakur
Andrij Holian
University of Montana · USCenter for Environmental Health · US

Funding

THE ROLE OF PULMONARY SUBPOPULATIONS AND TH2 IMMUNITY IN BALB/C SILICOSIS MODELP20RR017670 · NCRR · UNIVERSITY OF MONTANA · PI ROBERTS, KEVAN · 2002 to 2011
$22.0M
Molecular Histology and Fluorescent ImagingP30GM103338 · NIGMS · UNIVERSITY OF MONTANA · PI HOLIAN, ANDRIJ · 2013 to 2017
$5.6M
Defining the roles of macrophages subsets and NK lymphocytes in silicosisR01ES015294 · NIEHS · UNIVERSITY OF MONTANA · PI HOLIAN, ANDRIJ · 2007 to 2011
$1.6M
NCRR NIH HHS P20 RR017670NCRR NIH HHS P20-RR-017670NIEHS NIH HHS ES 015294NIEHS NIH HHS R01 ES015294NIGMS NIH HHS P30 GM103338
6 · The paper itself

Abstract

Inhalation of the crystalline form of silica is associated with a variety of pathologies, from acute lung inflammation to silicosis, in addition to autoimmune disorders and cancer. Basic science investigators looking at the mechanisms involved with the earliest initiators of disease are focused on how the alveolar macrophage interacts with the inhaled silica particle and the consequences of silica-induced toxicity on the cellular level. Based on experimental results, several rationales have been developed for exactly how crystalline silica particles are toxic to the macrophage cell that is functionally responsible for clearance of the foreign particle. For example, silica is capable of producing reactive oxygen species (ROS) either directly (on the particle surface) or indirectly (produced by the cell as a response to silica), triggering cell-signaling pathways initiating cytokine release and apoptosis. With murine macrophages, reactive nitrogen species are produced in the initial respiratory burst in addition to ROS. An alternative explanation for silica toxicity includes lysosomal permeability, by which silica disrupts the normal internalization process leading to cytokine release and cell death. Still other research has focused on the cell surface receptors (collectively known as scavenger receptors) involved in silica binding and internalization. The silica-induced cytokine release and apoptosis are described as the function of receptor-mediated signaling rather than free radical damage. Current research ideas on silica toxicity and binding in the alveolar macrophage are reviewed and discussed.

Indexed as

AnimalsApoptosisFree RadicalsHumansLungLysosomesMacrophagesMacrophages, AlveolarMiceModels, BiologicalProtein BindingReactive Nitrogen SpeciesSignal TransductionSilicon DioxideSurface-Active AgentsFree RadicalsReactive Nitrogen SpeciesSilicon DioxideSurface-Active Agents

Identifiers

PMID18226603
PMCPMC2680955
OpenAlexW2044353844

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.