Evidence map›Paper›PMID 33509151›Full record

ArticleBMC pulmonary medicine2021

FSTL1 aggravates cigarette smoke-induced airway inflammation and airway remodeling by regulating autophagy.

Ying Liu, Jiawei Xu, Tian Liu, Jinxiang Wu, Jiping Zhao, Junfei Wang, Minfang Zou, Lili Cao, Xiaofei Liu, Yun Pan and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  4. Mechanisms Underlying Altitude-Induced and Group 3 Pulmonary Hypertension.International journal of molecular sciences · 2026
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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

12 authors at 2 institutions in 1 country.

Ying Liu *Department of Respiratory, Shandong Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Jiawei Xu *Department of Respiratory, Shandong Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Tian LiuDepartment of Respiratory and Critical Care Medicine, Qilu Hospital, Jinan, China.
Jinxiang WuDepartment of Respiratory and Critical Care Medicine, Qilu Hospital, Jinan, China.
Jiping ZhaoDepartment of Respiratory and Critical Care Medicine, Qilu Hospital, Jinan, China.
Junfei WangDepartment of Respiratory and Critical Care Medicine, Qilu Hospital, Jinan, China.
Minfang ZouDepartment of Respiratory and Critical Care Medicine, Qilu Hospital, Jinan, China.
Lili CaoDepartment of Respiratory, Shandong Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Xiaofei LiuDepartment of Respiratory, Shandong Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Yun PanDepartment of Respiratory, Shandong Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Siyuan HuangDepartment of Respiratory, Shandong Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Liang DongDepartment of Respiratory, Shandong Provincial Qianfoshan Hospital, Shandong University, The First Affiliated Hospital of Shandong First Medical University, Shandong Institute of Respiratory Diseases, #16766, Jingshi Road, Jinan CityShandong Province, 250014, China. dl5506@126.com.ORCID http://orcid.org/0000-0001-7707-9982
Shandong University · CNQilu Hospital of Shandong University · CN

Funding

National Natural Science Foundation of China Grant nos. 81770029
6 · The paper itself

Abstract

backgroundCigarette smoke (CS) is a major risk factor for Chronic Obstructive Pulmonary Disease (COPD). Follistatin-like protein 1 (FSTL1), a critical factor during embryogenesis particularly in respiratory lung development, is a novel mediator related to inflammation and tissue remodeling. We tried to investigate the role of FSTL1 in CS-induced autophagy dysregulation, airway inflammation and remodeling.

methodsSerum and lung specimens were obtained from COPD patients and controls. Adult female wild-type (WT) mice, FSTL1

resultsBoth FSTL1 and autophagy biomarkers increased in COPD patients and CS-exposed WT mice. Autophagy activation was upregulated in CS-exposed mice accompanied by airway remodeling and airway inflammation. FSTL1

conclusionsFSTL1 promotes CS-induced COPD by modulating autophagy, therefore targeting FSTL1 and autophagy may shed light on treating cigarette smoke-induced COPD.

Indexed as

AdenineAdultAirway RemodelingAnimalsAutophagyBiomarkersBronchoalveolar Lavage FluidCigarette SmokingCytokinesDisease Models, AnimalFemaleFollistatin-Related ProteinsHumansInflammationLungMale3-methyladenineAdenineBiomarkersCytokinesFollistatin-Related ProteinsFSTL1 protein, humanFstl1 protein, mouse3-methyladenineAutophagyChronic obstructive pulmonary diseaseFollistatin-like protein-1

Identifiers

PMID33509151
PMCPMC7841997
OpenAlexW3116928598

What OpenQuestion holds

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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.