Evidence map›Paper›PMID 28337301›Full record

ArticleAmerican journal of translational research2017

Endoplasmic reticulum stress, a new wrestler, in the pathogenesis of idiopathic pulmonary fibrosis.

Lei Zhang, Yi Wang, Nuruliarizki Shinta Pandupuspitasari, Guorao Wu, Xudong Xiang, Quan Gong, Weining Xiong, Cong-Yi Wang, Ping Yang, Boxu Ren

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 38 citations in OpenAlex.

  1. The ribosomal landscape in influenza A virus infection: from molecular mechanisms to clinical relevance.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  2. Review
  3. Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Healing after COVID-19: are survivors at risk for pulmonary fibrosis?American journal of physiology. Lung cellular and molecular physiology · 2021
    Review
  10. Article
  11. TGF-β Promotes Metabolic Reprogramming in Lung Fibroblasts via mTORC1-dependent ATF4 Activation.American journal of respiratory cell and molecular biology · 2020
    Article
  12. Update on the role of endoplasmic reticulum stress in asthma.American journal of translational research · 2020
    Review
  13. Article
  14. Review
  15. Article
  16. Characterization of CD28Mucosal immunology · 2019
    Article
  17. Article
  18. Observational
  19. Review
  20. Endoplasmic reticulum stress in pulmonary fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2018
    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

10 authors at 3 institutions in 1 country.

Lei ZhangThe Center for Biomedical Research, Key Laboratory of Organ Transplantation, Ministry of Education, Ministry of Health, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology Wuhan, China.
Yi WangThe Center for Biomedical Research, Key Laboratory of Organ Transplantation, Ministry of Education, Ministry of Health, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology Wuhan, China.
Nuruliarizki Shinta PandupuspitasariThe Center for Biomedical Research, Key Laboratory of Organ Transplantation, Ministry of Education, Ministry of Health, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology Wuhan, China.
Guorao WuThe Center for Biomedical Research, Key Laboratory of Organ Transplantation, Ministry of Education, Ministry of Health, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology Wuhan, China.
Xudong XiangDepartment of Emergency Medicine, Institute of Emergency Medicine and Rare Diseases, The Second Xiangya Hospital, Central South University Changsha, China.
Quan GongClinical and Molecular Immunology Research Center, Department of Immunology, Medical College of Yangtze University Jingzhou, Hubei, China.
Weining XiongThe Center for Biomedical Research, Key Laboratory of Organ Transplantation, Ministry of Education, Ministry of Health, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology Wuhan, China.
Cong-Yi WangThe Center for Biomedical Research, Key Laboratory of Organ Transplantation, Ministry of Education, Ministry of Health, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology Wuhan, China.
Ping YangThe Center for Biomedical Research, Key Laboratory of Organ Transplantation, Ministry of Education, Ministry of Health, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology Wuhan, China.
Boxu RenClinical and Molecular Immunology Research Center, Department of Immunology, Medical College of Yangtze University Jingzhou, Hubei, China.
Huazhong University of Science and Technology · CNYangtze University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) has attracted extensive attention for its unexplained progressive lung scarring, short median survival and its unresponsiveness to traditional therapies. Despite extensive studies, the mechanisms underlying IPF pathoetiologies, however, remain poorly understood. Recent advances delineated a potential function of endoplasmic reticulum (ER) stress in meeting the need of fibrotic response, which pinpointed a critical role for the unfolded protein response (UPR) pathways in IPF pathogenesis. In this review, we highlight the effect of ER stress and the activation of UPR on the survival, differentiation, function and proliferation of major profibrotic cells in lung tissues during the course of IPF, and discuss the feasibility whether targeting UPR components could be an orientation for developing effective therapeutic strategies against this devastating disorder in clinical settings.

Indexed as

ER stressIPFpathogenesisprofibrotic cellsUPR

Identifiers

PMID28337301
PMCPMC5340708
OpenAlexW2970426266

What OpenQuestion holds

Textmetadata
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.