Evidence map›Paper›PMID 36468453›Full record

ReviewTherapeutic advances in respiratory disease

The role of autophagy in idiopathic pulmonary fibrosis: from mechanisms to therapies.

Yue-Liang Yue, Meng-Yu Zhang, Jian-Yu Liu, Li-Jun Fang, Yi-Qing Qu

Open access · goldAbstract readReview
In one paragraph

Review in Therapeutic advances in respiratory disease. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

43 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Aspirin Attenuates Liver Fibrosis via Autophagy Induction.Journal of cellular and molecular medicine · 2025
    Article
  20. Article
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

5 authors at 1 institution in 1 country.

Yue-Liang YueShandong Key Laboratory of Infectious Respiratory Diseases, Laboratory of Basic Medical Sciences, Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, China.
Meng-Yu ZhangShandong Key Laboratory of Infectious Respiratory Diseases, Laboratory of Basic Medical Sciences, Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, China.
Jian-Yu LiuShandong Key Laboratory of Infectious Respiratory Diseases, Laboratory of Basic Medical Sciences, Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, China.
Li-Jun FangShandong Key Laboratory of Infectious Respiratory Diseases, Laboratory of Basic Medical Sciences, Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Jinan, China.
Yi-Qing QuShandong Key Laboratory of Infectious Respiratory Diseases, Laboratory of Basic Medical Sciences, Department of Pulmonary and Critical Care Medicine, Qilu Hospital of Shandong University, Wenhuaxi Road 107#, Jinan 250012, China.ORCID 0000-0002-9538-7601
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is an interstitial pulmonary disease with an extremely poor prognosis. Autophagy is a fundamental intracellular process involved in maintaining cellular homeostasis and regulating cell survival. Autophagy deficiency has been shown to play an important role in the progression of pulmonary fibrosis. This review focused on the six steps of autophagy, as well as the interplay between autophagy and other seven pulmonary fibrosis related mechanisms, which include extracellular matrix deposition, myofibroblast differentiation, epithelial-mesenchymal transition, pulmonary epithelial cell dysfunction, apoptosis, TGF-β1 pathway, and the renin-angiotensin system. In addition, this review also summarized autophagy-related signaling pathways such as mTOR, MAPK, JAK2/STAT3 signaling, p65, and Keap1/Nrf2 signaling during the development of IPF. Furthermore, this review also illustrated the commonly used autophagy detection methods, the currently approved antifibrotic drugs pirfenidone and nintedanib, and several prospective compounds targeting autophagy for the treatment of IPF.

Indexed as

Idiopathic Pulmonary FibrosisAutophagyHumansKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Prospective StudiesKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2autophagyautophagy detectionidiopathic pulmonary fibrosistherapies

Identifiers

PMID36468453
PMCPMC9726854
OpenAlexW4311578428

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.