Evidence map›Paper›PMID 37760828›Full record

ReviewBiomedicines2023

HSP47: A Therapeutic Target in Pulmonary Fibrosis.

Noriho Sakamoto, Daisuke Okuno, Takatomo Tokito, Hirokazu Yura, Takashi Kido, Hiroshi Ishimoto, Yoshimasa Tanaka, Hiroshi Mukae

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
7.2field-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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Around the collagen triple helix: an introduction to studying associated genetic and acquired diseases.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Review
  7. Emerging Concepts in Therapeutic Interventions for Idiopathic Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Insights into the Mechanism of Action of the Degraded Limonoid Prieurianin.International journal of molecular sciences · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. 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

8 authors at 1 institution in 1 country.

Noriho SakamotoDepartment of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.ORCID 0000-0002-7577-476X
Daisuke OkunoDepartment of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Takatomo TokitoDepartment of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Hirokazu YuraDepartment of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Takashi KidoDepartment of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.ORCID 0000-0001-8338-0608
Hiroshi IshimotoDepartment of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.ORCID 0000-0002-4374-2894
Yoshimasa TanakaCenter for Medical Innovation, Nagasaki University, Nagasaki 852-8588, Japan.ORCID 0000-0002-5024-0614
Hiroshi MukaeDepartment of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Nagasaki University · JP

Funding

Non-profit Organization Aimed to Support Community Medicine Research in Nagasaki 3502
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by a progressive decline in lung function and poor prognosis. The deposition of the extracellular matrix (ECM) by myofibroblasts contributes to the stiffening of lung tissue and impaired oxygen exchange in IPF. Type I collagen is the major ECM component and predominant collagen protein deposited in chronic fibrosis, suggesting that type I collagen could be a target of drugs for fibrosis treatment. Heat shock protein 47 (HSP47), encoded by the serpin peptidase inhibitor clade H, member 1 gene, is a stress-inducible collagen-binding protein. It is an endoplasmic reticulum-resident molecular chaperone essential for the correct folding of procollagen. HSP47 expression is increased in cellular and animal models of pulmonary fibrosis and correlates with pathological manifestations in human interstitial lung diseases. Various factors affect HSP47 expression directly or indirectly in pulmonary fibrosis models. Overall, understanding the relationship between HSP47 expression and pulmonary fibrosis may contribute to the development of novel therapeutic strategies.

Indexed as

alveolar epithelial cellanti-fibrotic agentchaperoncollagenfibroblastheat shock protein 47pulmonary fibrosisSERPINH1

Identifiers

PMID37760828
PMCPMC10525413
OpenAlexW4386222650

What OpenQuestion holds

Textmetadata
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.