Evidence map›Paper›PMID 36166308›Full record

ArticleJCI insight2022

Liposomal UHRF1 siRNA shows lung fibrosis treatment potential through regulation of fibroblast activation.

Demin Cheng, Yue Wang, Ziwei Li, Haojie Xiong, Wenqing Sun, Sichuan Xi, Siyun Zhou, Yi Liu, Chunhui Ni

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Pulmonary fibrosis: from mechanisms to therapies.Journal of translational medicine · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Crosstalk of ubiquitin system and non-coding RNA in fibrosis.International journal of biological sciences · 2024
    Review
  13. Review
  14. 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

9 authors at 3 institutions in 3 countries.

Demin ChengDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology, Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China.
Yue WangDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology, Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China.
Ziwei LiDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology, Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China.
Haojie XiongDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology, Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China.
Wenqing SunDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology, Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China.
Sichuan XiThoracic Epigenetics Section, Thoracic Surgery Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Siyun ZhouDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology, Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China.
Yi LiuGusu School, Nanjing Medical University, Nanjing, China.
Chunhui NiDepartment of Occupational Medical and Environmental Health, Key Laboratory of Modern Toxicology, Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China.
Ministry of Education · KRNanjing Medical University · CNNational Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis is a chronic and progressive interstitial lung disease associated with the decay of pulmonary function, which leads to a fatal outcome. As an essential epigenetic regulator of DNA methylation, the involvement of ubiquitin-like containing PHD and RING finger domains 1 (UHRF1) in fibroblast activation remains largely undefined in pulmonary fibrosis. In the present study, we found that TGF-β1-mediated upregulation of UHRF1 repressed beclin 1 via methylated induction of its promoter, which finally resulted in fibroblast activation and lung fibrosis both in vitro and in vivo. Moreover, knockdown of UHRF1 significantly arrested fibroblast proliferation and reactivated beclin 1 in lung fibroblasts. Thus, intravenous administration of UHRF1 siRNA-loaded liposomes significantly protected mice against experimental pulmonary fibrosis. Accordingly, our data suggest that UHRF1 might be a novel potential therapeutic target in the pathogenesis of pulmonary fibrosis.

Indexed as

CCAAT-Enhancer-Binding ProteinsPulmonary FibrosisAnimalsFibroblastsMiceRNA, Small InterferingUbiquitin-Protein LigasesCCAAT-Enhancer-Binding ProteinsRNA, Small InterferingUbiquitin-Protein LigasesUhrf1 protein, mouseFibrosisPulmonology

Identifiers

PMID36166308
PMCPMC9746815
OpenAlexW4297249987

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.