Evidence map›Paper›PMID 41413225›Full record

ArticleScientific reports2025

Polyacrylic acid, but not polyethylene glycol, induces metabolic reprogramming linked to pulmonary fibrosis in rats.

Taisuke Tomonaga, Hiroto Izumi, Chinatsu Nishida, Kazuma Sato, Yuiko Nakamura, Shinya Morimoto, Toshiki Morimoto, Yasuyuki Higashi, Hidenori Higashi, Midori Iida and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

16 authors.

Taisuke TomonagaDepartment of Occupational Pneumology, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, 807-8555, Fukuoka, Japan. t-tomonaga@med.uoeh-u.ac.jp.
Hiroto IzumiDepartment of Occupational Pneumology, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, 807-8555, Fukuoka, Japan.
Chinatsu NishidaDepartment of Environmental Health Engineering, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan. 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, 807-8555, Fukuoka, Japan.
Kazuma SatoDepartment of Occupational Pneumology, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, 807-8555, Fukuoka, Japan.
Yuiko NakamuraDepartment of Occupational Pneumology, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, 807-8555, Fukuoka, Japan.
Shinya MorimotoDepartment of Occupational Pneumology, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, 807-8555, Fukuoka, Japan.
Toshiki MorimotoDepartment of Respiratory Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, 807-8555, Fukuoka, Japan.
Yasuyuki HigashiDepartment of Respiratory Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, 807-8555, Fukuoka, Japan.
Hidenori HigashiDepartment of Environmental Health Engineering, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan. 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, 807-8555, Fukuoka, Japan.
Midori IidaDepartment of Physics and Information Technology, Kyushu Institute of Technology, 680-4 Kawazu, Iizuka-shi, Fukuoka, 820-8502, Japan.
Takuma KojimaDepartment of Chemistry and Biochemistry, The University of Kitakyushu, 1-1, Hibikino, Wakamatsu-ku, Kitakyushu, 808-0135, Fukuoka, Japan.
Kazuo SakuraiDepartment of Chemistry and Biochemistry, The University of Kitakyushu, 1-1, Hibikino, Wakamatsu-ku, Kitakyushu, 808-0135, Fukuoka, Japan.
Akihiro MoriyamaResearch Institute of Science for Safety and Sustainability, National Institute of Advanced Industrial Science and Technology (AIST), 16-1 Onogawa, Tsukuba, Tsukuba, 305-8569, Ibaraki, Japan.
Jun-Ichi TakeshitaResearch Institute of Science for Safety and Sustainability, National Institute of Advanced Industrial Science and Technology (AIST), 16-1 Onogawa, Tsukuba, Tsukuba, 305-8569, Ibaraki, Japan.
Kazuhiro YateraDepartment of Respiratory Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, 807-8555, Fukuoka, Japan.
Yasuo MorimotoDepartment of Occupational Pneumology, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahata-nishi-ku, Kitakyushu, 807-8555, Fukuoka, Japan.

Funding

Japan Society for the Promotion of Science JP21H04855
6 · The paper itself

Abstract

Polyacrylic acids are widely used in industrial and consumer products, yet increasing evidence indicates that they can induce severe lung injury and rapidly progressing fibrosis. The underlying mechanisms remain unclear. In this study, we investigated the pulmonary toxicity of polyacrylic acid (A45) in comparison with polyethylene glycol (PEG, negative control) in a rat intratracheal instillation model. Lung inflammation and fibrosis were assessed up to 6 months. To explore systemic responses to pulmonary injury, serum metabolomics was performed using capillary electrophoresis time-of-flight mass spectrometry (CE-TOFMS). A45 exposure caused marked neutrophil infiltration, elevated inflammatory markers, and persistent fibrotic remodeling, while PEG induced no significant pulmonary changes. Metabolomic profiling detected 249 metabolites, of which 182 passed quality filtering. A45 significantly altered amino acid, energy, and redox pathways, whereas PEG showed minimal changes. Differential metabolites included valine, leucine, alanine, glutamine, malate, carnitine, cysteine, and methionine sulfoxide. Pathway analysis revealed enrichment of amino-acid/collagen-related and energy-demanding pathways. These findings demonstrate that polyacrylic acid induces systemic metabolic reprogramming linked to oxidative stress, mitochondrial dysfunction, and fibrosis, highlighting serum metabolomics as a valuable tool for mechanistic toxicology and biomarker discovery.

Indexed as

Acrylic ResinsPolyethylene GlycolsPulmonary FibrosisAnimalsBiomarkersDisease Models, AnimalLungMaleMetabolic ReprogrammingMetabolomeMetabolomicsOxidative StressRatsRats, Sprague-DawleyAcrylic ResinsBiomarkerscarbopol 940Polyethylene GlycolsFibrosisIntratracheal instillationMetabolomicsPolyacrylic acidPolyethylene glycolRat

Identifiers

PMID41413225
PMCPMC12830845

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Registered trials

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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.