Evidence map›Paper›PMID 41794752›Full record

ArticleParticle and fibre toxicology2026

Inhibition of PADI2-mediated vimentin citrullination alleviates silica-induced pulmonary fibrosis in mice.

Fuyu Jin, Yaqian Li, Tian Li, Shupeng Liu, Dingjie Xu, Heliang Liu, Zhongqiu Wei, Xuemin Gao, Na Mao, Wenchen Cai and 3 more

Abstract read
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In one paragraph

Article in Particle and fibre toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Fuyu Jin *School of Public Health, Hebei Key Laboratory for Organ Fibrosis Research, North China University of Science and Technology, Tangshan, China.
Yaqian Li *College of TCM, North China University of Science and Technology, Tangshan, 063210, Hebei Province, China.
Tian Li *School of Public Health, Hebei Key Laboratory for Organ Fibrosis Research, North China University of Science and Technology, Tangshan, China.
Shupeng LiuSchool of Public Health, Hebei Key Laboratory for Organ Fibrosis Research, North China University of Science and Technology, Tangshan, China.
Dingjie XuCollege of TCM, North China University of Science and Technology, Tangshan, 063210, Hebei Province, China.
Heliang LiuSchool of Public Health, Hebei Key Laboratory for Organ Fibrosis Research, North China University of Science and Technology, Tangshan, China.
Zhongqiu WeiSchool of Public Health, Hebei Key Laboratory for Organ Fibrosis Research, North China University of Science and Technology, Tangshan, China.
Xuemin GaoSchool of Public Health, Hebei Key Laboratory for Organ Fibrosis Research, North China University of Science and Technology, Tangshan, China.
Na MaoSchool of Public Health, Hebei Key Laboratory for Organ Fibrosis Research, North China University of Science and Technology, Tangshan, China.
Wenchen CaiSchool of Public Health, Hebei Key Laboratory for Organ Fibrosis Research, North China University of Science and Technology, Tangshan, China.
Yiwei ShiNHC Key Laboratory of Pneumoconiosis, Department of Pulmonary and Critical Care Medicine, The First Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi province, China. chinasyw225@163.com.
Haibo ZhangDepartment of Anesthesiology and Pain Medicine, Department of Physiology, Interdepartmental Division of Critical Care Medicine, University of Toronto, Toronto, ON, Canada. hzhaibozhang@gmail.com.
Hong XuSchool of Public Health, Hebei Key Laboratory for Organ Fibrosis Research, North China University of Science and Technology, Tangshan, China. xuhong@ncst.edu.cn.

Funding

National Natural Science Foundation of China 82473607
6 · The paper itself

Abstract

Silicosis remains a critical occupational health concern worldwide, lacking effective treatments due to unclear mechanisms. In this study, we investigated the citrullinated proteomic profile and its effects in mice exposed to silica. Our findings demonstrated elevated levels of citrullinated peptides and citrullinated vimentin (Cit-Vim) in silicotic mice and silica-treated macrophages, regulated by peptidylarginine deiminase (PADI2). Unlike vimentin, Cit-Vim amplified the production of tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6), and IL-1β in silica-treated macrophages through interaction with Toll-like receptor 4 (TLR4) signaling. RNA sequencing revealed that early growth response protein 1 (EGR1) is a target of PADI2, with Cit-Vim inducing lung inflammation via EGR1 signaling. Pharmacological inhibition or genetic knockout of Padi2 attenuated silica-induced lung inflammation and fibrosis. These findings suggest that targeting PADI2 may represent a novel therapeutic strategy of silicosis.

Indexed as

CitrullinationProtein-Arginine Deiminase Type 2Pulmonary FibrosisSilicon DioxideSilicosisVimentinAnimalsCytokinesEarly Growth Response Protein 1LungMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutProtein-Arginine DeiminasesCytokinesEarly Growth Response Protein 1Egr1 protein, mousePadi2 protein, mouseProtein-Arginine DeiminasesProtein-Arginine Deiminase Type 2Silicon DioxideVimentinVim protein, mouseCitrullinated vimentinEarly growth response protein 1Peptidylarginine deiminasesSilicosis

Identifiers

PMID41794752
PMCPMC13019754

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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.