Evidence map›Paper›PMID 35216634›Full record

ArticleCell & bioscience2022

A missing piece of the puzzle in pulmonary fibrosis: anoikis resistance promotes fibroblast activation.

Juan Yin, Jing Wang, Xinxin Zhang, Yan Liao, Wei Luo, Sha Wang, Jiawei Ding, Jie Huang, Mengling Chen, Wei Wang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

10 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 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 3 institutions in 2 countries.

Juan Yin *Jiangsu Provincial Key Laboratory of Critical Care Medicine, Zhongda Hospital, Department of Physiology, School of Medicine, Southeast University, #87 Dingjiaqiao Rd, Nanjing, 210009, Jiangsu, China.
Jing Wang *Jiangsu Provincial Key Laboratory of Critical Care Medicine, Zhongda Hospital, Department of Physiology, School of Medicine, Southeast University, #87 Dingjiaqiao Rd, Nanjing, 210009, Jiangsu, China.
Xinxin Zhang *Jiangsu Provincial Key Laboratory of Critical Care Medicine, Zhongda Hospital, Department of Physiology, School of Medicine, Southeast University, #87 Dingjiaqiao Rd, Nanjing, 210009, Jiangsu, China.
Yan Liao *Jiangsu Provincial Key Laboratory of Critical Care Medicine, Zhongda Hospital, Department of Physiology, School of Medicine, Southeast University, #87 Dingjiaqiao Rd, Nanjing, 210009, Jiangsu, China.
Wei LuoJiangsu Provincial Key Laboratory of Critical Care Medicine, Zhongda Hospital, Department of Physiology, School of Medicine, Southeast University, #87 Dingjiaqiao Rd, Nanjing, 210009, Jiangsu, China.
Sha WangJiangsu Provincial Key Laboratory of Critical Care Medicine, Zhongda Hospital, Department of Physiology, School of Medicine, Southeast University, #87 Dingjiaqiao Rd, Nanjing, 210009, Jiangsu, China.
Jiawei DingJiangsu Provincial Key Laboratory of Critical Care Medicine, Zhongda Hospital, Department of Physiology, School of Medicine, Southeast University, #87 Dingjiaqiao Rd, Nanjing, 210009, Jiangsu, China.
Jie HuangJiangsu Provincial Key Laboratory of Critical Care Medicine, Zhongda Hospital, Department of Physiology, School of Medicine, Southeast University, #87 Dingjiaqiao Rd, Nanjing, 210009, Jiangsu, China.
Mengling ChenJiangsu Provincial Key Laboratory of Critical Care Medicine, Zhongda Hospital, Department of Physiology, School of Medicine, Southeast University, #87 Dingjiaqiao Rd, Nanjing, 210009, Jiangsu, China.
Wei WangDepartment of Respiratory Medicine, Nanjing Chest Hospital, the Affiliated Brain Hospital of Nanjing Medical University, Nanjing, 210029, Jiangsu, China. z_1998spirit1980@163.com.
Shencun FangDepartment of Respiratory Medicine, Nanjing Chest Hospital, the Affiliated Brain Hospital of Nanjing Medical University, Nanjing, 210029, Jiangsu, China. fang1984@aliyun.com.
Jie ChaoJiangsu Provincial Key Laboratory of Critical Care Medicine, Zhongda Hospital, Department of Physiology, School of Medicine, Southeast University, #87 Dingjiaqiao Rd, Nanjing, 210009, Jiangsu, China. chaojie@seu.edu.cn.ORCID http://orcid.org/0000-0002-7800-3557
Zhongda Hospital Southeast University · CNNanjing Brain Hospital · CNXizang Minzu University · CN

Funding

National Key R&D Program of China 2017YFA0104303National Natural Science Foundation of China 81773796National Natural Science Foundation of China 81972987Natural Science Foundation of Shanghai 81700068
6 · The paper itself

Abstract

backgroundPulmonary fibrosis initiates a pneumonic cascade that leads to fibroblast dysfunction characterized by excess proliferation. Anoikis is a physiological process that ensures tissue development and homeostasis. Researchers have not clearly determined whether disruption of anoikis is involved in pulmonary fibrosis.

resultsHere, we investigated the mechanism by which silica induces fibroblast activation via anoikis resistance and subsequent fibrosis. Anoikis of lung fibroblasts, alveolar epithelial cells and endothelial cells during the process of fibrosis was detected using CCK-8, western blot, cell count and flow cytometry (FCM) assays. Although the three cell types showed similar increases in proliferation, the expression of NTRK2, a marker of anoikis resistance, was upregulated specifically in fibroblasts, indicating the unique proliferation mechanism of fibroblasts in pulmonary fibrosis, which may be related to anoikis resistance. Furthermore, the CRISPR/Cas9 system was used to investigate the molecular mechanism of anoikis resistance; the SiO

conclusionsThe current study revealed a specific pattern of fibroblast proliferation, and strategies targeting anoikis resistance may inhibit the pathological process of pulmonary fibrosis. This result provides a new approach for treating pulmonary fibrosis and new insights into the potential application of ZC3H4 in the development of novel therapeutic strategies for mitigating pulmonary fibrosis.

Indexed as

AnoikisECMFibroblastPulmonary fibrosisZC3H4

Identifiers

PMID35216634
PMCPMC8881884
OpenAlexW4220710679

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.