Evidence map›Paper›PMID 41519726›Full record

ArticleRespiratory research2026

Surfactant protein A deficiency aggravates silica-induced pulmonary fibrosis by promoting intrinsic apoptosis of alveolar type II epithelial cells.

Yali Lan, Ping Wang, Zhiming Hu, Wenyao Su, Yushi Ou, Jianlin Shen, Jiayin Feng, Huifan Yang, Ziping Zou, Zexian Dong and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Respiratory research, 2026. 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

15 authors.

Yali Lan *Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Ping Wang *Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Zhiming HuGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Wenyao SuGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Yushi OuGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Jianlin ShenSchool of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Jiayin FengGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Huifan YangGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Ziping ZouGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Zexian DongGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Chuifei ZhongGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Kengkeng ChenGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Xiaohui TanGuangzhou Key Laboratory of Forensic Multi-Omics for Precision Identification, School of Forensic Medicine, Southern Medical University, Guangzhou, 510515, China.
Yiru QinGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Na ZhaoGuangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China. zhaona@gdpcc.com.

Funding

Biomedical Industry Innovation Subsidy of Guangzhou Science and Technology Bureau 202302002Guangdong Medical Scientific Research Foundation A2025148the Natural Science Foundation of Guangdong Province, China 2023A1515010085Zhongnanshan Medical Foundation of Guangdong Province ZNSXS-20250029
6 · The paper itself

Abstract

backgroundSilicosis is an incurable occupational lung disease characterized by progressive fibrosis and respiratory failure, imposing a significant global health burden. Surfactant protein A (SP-A) plays a critical role in maintaining pulmonary homeostasis, yet its mechanistic role in silicosis remains unclear.

methodsSP-A expression was assessed in lung tissues from patients with silicosis and in silica-exposed mice. Sftpa1 gene knockout (Sftpa1

resultsSP-A levels were notably reduced in the lung tissue of silicosis patients and in experimental silicosis mice, correlating inversely with disease severity. Sftpa1

conclusionsThese findings demonstrate that SP-A deficiency exacerbates silica-induced pulmonary fibrosis by promoting epithelial apoptosis involving the Bcl-2/Bax/Caspase pathway, highlighting the role of SP-A in fibrogenesis progression and providing a basis for its potential therapeutic target for silicosis.

Indexed as

Alveolar Epithelial CellsApoptosisPulmonary FibrosisPulmonary Surfactant-Associated Protein ASilicon DioxideSilicosisA549 CellsAnimalsHumansMaleMiceMice, Inbred C57BLMice, KnockoutPulmonary Surfactant-Associated Protein ASFTPA1 protein, humanSilicon DioxideAEC IIApoptosisSftpa1 -/- miceSilicaSP-A

Identifiers

PMID41519726
PMCPMC12879440

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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.