Evidence map›Paper›PMID 28024734›Full record

ArticleEBioMedicine2017

Lyn kinase represses mucus hypersecretion by regulating IL-13-induced endoplasmic reticulum stress in asthma.

Xing Wang, Xiaoqiong Yang, Yin Li, Xiaoyun Wang, Yun Zhang, Xi Dai, Bin Niu, Juan Wu, Xiefang Yuan, Anjie Xiong and 4 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  8. Frontiers in immunology · 2025
    Review
  9. Article
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  11. Article
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  13. Article
  14. Article
  15. Endoplasmic reticulum stress: a vital process and potential therapeutic target in chronic obstructive pulmonary disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  16. Article
  17. Article
  18. Review
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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

14 authors at 5 institutions in 3 countries.

Xing WangInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Xiaoqiong YangInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Yin LiThe First Clinic College, Chongqing Medical University, Chongqing 401331, China.
Xiaoyun WangInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Yun ZhangState Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macao, China.
Xi DaiState Key Laboratory of Quality Research in Chinese Medicine, Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macao, China.
Bin NiuInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Juan WuFirst Department of Respiratory Disease, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Xiefang YuanInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Anjie XiongInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Zhigang LiuInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China; State Key Laboratories of Respiratory Disease, Ghuangzhou Medical University, Guangdong 510120, China.
Nanshan ZhongState Key Laboratories of Respiratory Disease, Ghuangzhou Medical University, Guangdong 510120, China. Electronic address: Nanshan@vip.163.com.
Min WuDepartment of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, 1301 N Columbia Rd, Grand Forks, ND 58203-9037, United States. Electronic address: min.wu@med.und.edu.
Guoping LiInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China; First Department of Respiratory Disease, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China. Electronic address: lzlgp@163.com.
Affiliated Hospital of Southwest Medical University · CNMacau University of Science and Technology · MOState Key Laboratory of Respiratory Disease · CNChongqing Medical University · CNUniversity of North Dakota · US

Funding

Lung innate immunity against bacterial infectionR01AI109317 · NIAID · UNIVERSITY OF NORTH DAKOTA · PI WU, MIN · 2014 to 2018
$1.7M
Lung epithelium collaborates with alveolar macrophages in host defenseR15AI101973 · NIAID · UNIVERSITY OF NORTH DAKOTA · PI WU, MIN · 2012 to 2012
$414k
NIAID NIH HHS R01 AI109317NIAID NIH HHS R15 AI101973
6 · The paper itself

Abstract

In asthma, mucus hypersecretion is thought to be a prominent pathological feature associated with widespread mucus plugging. However, the current treatments for mucus hypersecretion are often ineffective or temporary. The potential therapeutic targets of mucus hypersecretion in asthma remain unknown. Here, we show that Lyn is a central effector of endoplasmic reticulum stress (ER stress) and mucous hypersecretion in asthma. In Lyn-transgenic mice (Lyn-TG) and wild-type (WT) C57BL/6J mice exposed to ovalbumin (OVA), Lyn overexpression attenuates mucus hypersecretion and ER stress. Interleukin 13 (IL-13) induced MUC5AC expression by enhancing ER stress in vitro. Lyn serves as a negative regulator of IL-13-induced ER stress and MUC5AC expression. We further find that an inhibitor of ER stress, which is likely involved in the PI3K p85α/Akt pathway and NFκB activity, blocked MUC5AC expression in Lyn-knockdown cells. Furthermore, PI3K/Akt signaling is required for IL-13-induced ER stress and MUC5AC expression in airway epithelial cells. The ER stress regulation of MUC5AC expression depends on NFκB in Lyn-knockdown airway epithelial cells. Our studies indicate not only a concept of mucus hypersecretion in asthma that involves Lyn kinase but also an important therapeutic candidate for asthma.

Indexed as

Endoplasmic Reticulum StressAnimalsAsthmaBiomarkersCase-Control StudiesCytokinesDisease Models, AnimalFemaleGene Knockdown TechniquesHumansInterleukin-13MaleMiceMice, TransgenicModels, BiologicalMucin 5ACBiomarkersCytokinesInterleukin-13lyn protein-tyrosine kinaseMucin 5ACNF-kappa BOvalbuminPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktsrc-Family KinasesAsthmaEndoplasmic reticulum stressLyn kinaseMUC5ACMucus secretion

Identifiers

PMID28024734
PMCPMC5233819
OpenAlexW2561400033

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.