Evidence map›Paper›PMID 30453980›Full record

ArticleRespiratory research2018

Role of SOD3 in silica-related lung fibrosis and pulmonary vascular remodeling.

Igor N Zelko, Jianxin Zhu, Jesse Roman

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. The TIMP protein family: diverse roles in pathophysiology.American journal of physiology. Cell physiology · 2024
    Review
  10. The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Anti-oxidative effects of superoxide dismutase 3 on inflammatory diseases.Journal of molecular medicine (Berlin, Germany) · 2020
    Review
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 1 institution in 1 country.

Igor N ZelkoDepartment of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, University of Louisville, 505 S. Hancock Street, CTR Bldg., room 524, Louisville, KY, 40202, USA. igor.zelko@louisville.edu.ORCID http://orcid.org/0000-0003-3976-3884
Jianxin ZhuDepartment of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, University of Louisville, 505 S. Hancock Street, CTR Bldg., room 524, Louisville, KY, 40202, USA.
Jesse RomanDepartment of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, University of Louisville, 505 S. Hancock Street, CTR Bldg., room 524, Louisville, KY, 40202, USA.
University of Louisville · US

Funding

Epigenetic regulation of EC-SOD in pulmonary hypertension related to lung fibrosisR56HL128597 · NHLBI · UNIVERSITY OF LOUISVILLE · PI ZELKO, IGOR N. · 2015 to 2015
$366k
Nicotine-induced fibronectin expression in lung injury and repairI01BX000216 · VA · VETERANS HEALTH ADMINISTRATION · PI ROMAN, JESSE · 2009 to 2018
–
BLRD VA I01 BX000216National Heart, Lung, and Blood Institute R56HL128597NHLBI NIH HHS R56 HL128597Office of Academic Affiliations, Department of Veterans Affairs BX000216
6 · The paper itself

Abstract

backgroundWork-place exposure to silica dust may lead to progressive lung inflammation culminating in the development of silicosis, an irreversible condition that can be complicated by onset of pulmonary hypertension (PH). The molecular mechanisms leading to the development of PH and lung fibrosis in response to silica are not well understood. Oxidant/antioxidant imbalance in the lung may promote fibroproliferation and vascular smooth muscle proliferation, ultimately leading to the development of PH. Herein, we analyze the development of PH and lung fibrosis in mice deficient in extracellular superoxide dismutase (SOD3), an enzyme with anti-oxidant activity.

methodsPH and silicosis were induced in wild-type and Sod3

resultsC57BL6 mice exposed to silica showed attenuated expression of Sod3 in the lung suggesting a protective role for Sod3. Consistent with this, Sod3

conclusionsOur data suggest that Sod3 and extracellular oxidative stress may play an important role in the development of pneumoconiosis and pulmonary vascular remodeling following exposure to environmental and occupational silica.

Indexed as

AnimalsMaleMiceMice, Inbred C57BLMice, KnockoutOxidative StressPulmonary FibrosisSilicon DioxideSuperoxide DismutaseVascular RemodelingSilicon DioxideSod3 protein, mouseSuperoxide DismutaseCrystalline silicaExpressionLung fibrosisOxidative stressPneumoconiosisPulmonary hypertensionSilicosisTranscription

Identifiers

PMID30453980
PMCPMC6245633
OpenAlexW2901813854

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.