Evidence map›Paper›PMID 33533071›Full record

ReviewThe journal of gene medicine2021

Long non-coding RNAs: Promising new targets in pulmonary fibrosis.

Songzi Zhang, Hongbin Chen, Dayong Yue, Timothy S Blackwell, Changjun Lv, Xiaodong Song

Open access · hybridAbstract readReview
In one paragraph

Review in The journal of gene medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Silicosis: from pathogenesis to therapeutics.Frontiers in pharmacology · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Epigenetic Changes and Functions in Pneumoconiosis.Oxidative medicine and cellular longevity · 2022
    Review
  18. Review
  19. Article
  20. 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

6 authors at 2 institutions in 2 countries.

Songzi ZhangDepartment of Cellular and Genetic Medicine, School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.
Hongbin ChenDepartment of Cellular and Genetic Medicine, School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.
Dayong YueDepartment of Cellular and Genetic Medicine, School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.
Timothy S BlackwellVanderbilt University Medical Center, Nashville, TN, USA.
Changjun LvDepartment of Cellular and Genetic Medicine, School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.
Xiaodong SongDepartment of Cellular and Genetic Medicine, School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, China.ORCID 0000-0003-2543-1790
Binzhou Medical University · CNVanderbilt University Medical Center · US

Funding

Mechanisms of Familial Pulmonary FibrosisP01HL092870 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BLACKWELL, TIMOTHY S. · 2010 to 2020
$21.6M
Thromboxane Receptor Signaling in Pulmonary FibrosisR01HL151016 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KROPSKI, JONATHAN ANDREW · 2020 to 2023
$2.1M
Important Project of Reasearch and Development of Shandong Province 2019GSF108040National Institute of Health P01HL092870National Natural Science Foundation of China 31670365National Natural Science Foundation of China 81670064National Natural Science Foundation of China 81741170National Natural Science Foundation of China 81870001National Natural Science Foundation of China 81970064NHLBI NIH HHS P01 HL092870NHLBI NIH HHS R01 HL151016
6 · The paper itself

Abstract

Pulmonary fibrosis is characterized by progressive and irreversible scarring in the lungs with poor prognosis and treatment. It is caused by various factors, including environmental and occupational exposures, and some rheumatic immune diseases. Even the rapid global spread of the COVID-19 pandemic can also cause pulmonary fibrosis with a high probability. Functions attributed to long non-coding RNAs (lncRNAs) make them highly attractive diagnostic and therapeutic targets in fibroproliferative diseases. Therefore, an understanding of the specific mechanisms by which lncRNAs regulate pulmonary fibrotic pathogenesis is urgently needed to identify new possibilities for therapy. In this review, we focus on the molecular mechanisms and implications of lncRNAs targeted protein-coding and non-coding genes during pulmonary fibrogenesis, and systematically analyze the communication of lncRNAs with various types of RNAs, including microRNA, circular RNA and mRNA. Finally, we propose the potential approach of lncRNA-based diagnosis and therapy for pulmonary fibrosis. We hope that understanding these interactions between protein-coding and non-coding genes will contribute to the development of lncRNA-based clinical applications for pulmonary fibrosis.

Indexed as

Gene Expression RegulationGenetic MarkersGenetic TherapyHumansMicroRNAsProteinsPulmonary FibrosisRNA, CircularRNA, Long NoncodingGenetic MarkersMicroRNAsProteinsRNA, CircularRNA, Long Noncodingcircular RNACOVID-19lncRNAmicroRNApulmonary fibrosis

Identifiers

PMID33533071
PMCPMC7988597
OpenAlexW3126207418

What Socratic 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 Socratic graph.