ArticleBiological trace element research2025
Mechanistic Insights Into the Role of Selenoprotein M in Nickel-Induced Lung Fibrosis.
Article in Biological trace element research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- The Protective Effects of Selenium Nanoparticles Against Metal Toxicity.Biological trace element research · 2026Review
- Research progress on molecular mechanisms and signaling pathways of toxic metal exposure-induced lung fibrosis.Frontiers in immunology · 2026Review
- Dietary Selenium-Enriched Aquatic Products for Human Health.Nutrients · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Long-term exposure to high concentrations of nickel (Ni) compounds could cause damage to lung tissue and increase the risk of lung and respiratory cancers. Selenoprotein M (SELENOM) plays a crucial role in antioxidant and anti-inflammatory activities. However, the relationship between SELENOM and the mechanism of Ni-induced pulmonary fibrosis in mice remains unknown. Our study explored the regulated mechanism of SELENOM in Ni-induced pulmonary fibrosis. Wild-type and SELENOM knockout C57BL/6N male mice were randomly divided into Wild-control and Wild-Ni groups, which were administered distilled water and NiCl
Indexed as
Identifiers
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Registered trials
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