Evidence map›Paper›PMID 29769446›Full record

ReviewJCI insight2018

Ubiquitination and deubiquitination emerge as players in idiopathic pulmonary fibrosis pathogenesis and treatment.

Shuang Li, Jing Zhao, Dong Shang, Daniel J Kass, Yutong Zhao

Open access · goldAbstract readReview
In one paragraph

Review in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
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  9. Review
  10. Review
  11. Article
  12. Targeting USP11 counteractsTheranostics · 2025
    Article
  13. Article
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  15. Article
  16. Review
  17. Article
  18. Article
  19. Epigenetics alternation in lung fibrosis and lung cancer.Frontiers in cell and developmental biology · 2022
    Review
  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 2 institutions in 2 countries.

Shuang LiDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Jing ZhaoDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Dong ShangDepartment of General Surgery, the First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Daniel J KassDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Yutong ZhaoDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
University of Pittsburgh · USDalian Medical University · CN

Funding

Twist1 subphenotypes and pulmonary fibrosisR01HL126990 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KASS, DANIEL J · 2015 to 2019
$1.9M
Molecular regulation of anti-inflammatory cytokine receptor in sepsisR01HL136294 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZHAO, YUTONG · 2018 to 2021
$1.8M
Regulation of proteolysis by deubiquiting enzyme in lung inflammatory diseaseR01HL131665 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZHAO, YUTONG · 2017 to 2020
$1.5M
Regulation of Histone Acetyltransferase Stability In SepsisR01GM115389 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZHAO, JING · 2015 to 2019
$1.5M
Regulation of the IL-33 receptor, ST2L, by Protein Stability in Septic InjuryR01HL112791 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZHAO, YUTONG · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL112791NHLBI NIH HHS R01 HL126990NHLBI NIH HHS R01 HL131665NHLBI NIH HHS R01 HL136294NIGMS NIH HHS R01 GM115389
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a fatal fibrotic lung disease that is associated with aberrant activation of TGF-β, myofibroblast differentiation, and abnormal extracellular matrix (ECM) production. Proper regulation of protein stability is important for maintenance of intracellular protein homeostasis and signaling. Ubiquitin E3 ligases mediate protein ubiquitination, and deubiquitinating enzymes (DUBs) reverse the process. The role of ubiquitin E3 ligases and DUBs in the pathogenesis of IPF is relatively unexplored. In this review, we provide an overview of how ubiquitin E3 ligases and DUBs modulate pulmonary fibrosis through regulation of both TGF-β-dependent and -independent pathways. We also summarize currently available small-molecule inhibitors of ubiquitin E3 ligases and DUBs as potential therapeutic strategies for the treatment of IPF.

Indexed as

HumansIdiopathic Pulmonary FibrosisTransforming Growth Factor betaUbiquitinationUbiquitin-Protein LigasesTransforming Growth Factor betaUbiquitin-Protein Ligases

Identifiers

PMID29769446
PMCPMC6012502
OpenAlexW2804647138

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.