Evidence map›Paper›PMID 30374330›Full record

ArticleFrontiers in endocrinology2018

IGFBP-5 Promotes Fibrosis via Increasing Its Own Expression and That of Other Pro-fibrotic Mediators.

Xinh-Xinh Nguyen, Lutfiyya Muhammad, Paul J Nietert, Carol Feghali-Bostwick

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.3field-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

56 citing papers in PubMed, 74 citations in OpenAlex.

  1. Trial
  2. Article
  3. Adaptation of mesenchymal stromal cells to culture on collagen-based bioscaffold.Journal of materials science. Materials in medicine · 2026
    Article
  4. Article
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  9. Article
  10. Review
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  12. Article
  13. The IGF System and Aging.Endocrine reviews · 2025
    Review
  14. Article
  15. IGF-II regulates lysyl oxidase propeptide and mediates its effects in part via basic helix-loop-helix E40.Matrix biology : journal of the International Society for Matrix Biology · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The Role of SOX9 in IGF-II-Mediated Pulmonary Fibrosis.International journal of molecular sciences · 2023
    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

4 authors at 1 institution in 1 country.

Xinh-Xinh NguyenDivision of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Lutfiyya MuhammadDepartment of Public Health Sciences, Medical University of South Carolina, Charleston, SC, United States.
Paul J NietertDepartment of Public Health Sciences, Medical University of South Carolina, Charleston, SC, United States.
Carol Feghali-BostwickDivision of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Medical University of South Carolina · US

Funding

South Carolina Clinical & Translational Research Institute (SCTR)UL1TR001450 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T., FLUME, PATRICK A · 2015 to 2024
$41.1M
Resource CoreP30AR072582 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JAMES C OATES · 2017 to 2026
$8.5M
South Carolina Clinical & Translational Research Institute (SCTR)TL1TR001451 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI FEGHALI-BOSTWICK, CAROL A. · 2015 to 2024
$4.6M
Mechanism of Action of Anti-Fibrotic PeptideR01HL121262 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI FEGHALI-BOSTWICK, CAROL A. · 2017 to 2020
$1.5M
Scleroderma Twin Study and analysis of Estrogen in patients with dcSScK24AR060297 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FEGHALI-BOSTWICK, CAROL A. · 2013 to 2025
$1.4M
NCATS NIH HHS TL1 TR001451NCATS NIH HHS UL1 TR001450NHLBI NIH HHS R01 HL121262NIAMS NIH HHS K24 AR060297NIAMS NIH HHS P30 AR072582
6 · The paper itself

Abstract

Pulmonary fibrosis is a hallmark of diseases such as systemic sclerosis (SSc, scleroderma) and idiopathic pulmonary fibrosis (IPF). To date, the therapeutic options for patients with pulmonary fibrosis are limited, and organ transplantation remains the most effective option. Insulin-like growth factor-binding protein 5 (IGFBP-5) is a conserved member of the IGFBP family of proteins that is overexpressed in SSc and IPF. In this study, we demonstrate that both exogenous and adenovirally expressed IGFBP-5 promote fibrosis by increasing the production of extracellular matrix (ECM) genes and the expression of pro-fibrotic genes in primary human lung fibroblasts. IGFBP-5 increased expression of the pro-fibrotic growth factor CTGF and levels of the matrix crosslinking enzyme lysyl oxidase (LOX). Silencing of IGFBP-5 had different effects in lung fibroblasts from normal donors and patients with SSc or IPF. Moreover, we show that IGFBP-5 increases expression of ECM genes, CTGF, and LOX in human lung tissues maintained in organ culture. Together, our data extend our previous findings and demonstrate that IGFBP-5 exerts its pro-fibrotic activity by directly inducing expression of ECM and pro-fibrotic genes. Further, IGFBP-5 promotes its own expression, generating a positive feedback loop. This suggests that IGFBP-5 likely acts in concert with other growth factors to drive fibrosis and tissue remodeling.

Indexed as

extracellular matrix (ECM)fibrosisidiopathic pulmonary fibrosis (IPF)insulin-like growth factor binding protein-5 (IGFBP-5)systemic sclerosis (SSc)

Identifiers

PMID30374330
PMCPMC6196226
OpenAlexW2896464224

What OpenQuestion holds

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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.