Evidence map›Paper›PMID 29941814›Full record

ReviewBiomedicines2018

Targeting TGFβ Signaling to Address Fibrosis Using Antisense Oligonucleotides.

James T March, Golnoush Golshirazi, Viktorija Cernisova, Heidi Carr, Yee Leong, Ngoc Lu-Nguyen, Linda J Popplewell

Abstract readReview
In one paragraph

Review in Biomedicines, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Article
  2. Review
  3. Fibrosis in Immune-Mediated and Autoimmune Disorders.Journal of clinical medicine · 2025
    Review
  4. Review
  5. Myostatin inhibition with orally administeredFrontiers in neurology · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Erythropoietin Alleviates Burn-induced Muscle Wasting.International journal of medical sciences · 2020
    Article
  14. Article
  15. Article
  16. Role of Transforming Growth Factor-β in Skeletal Muscle Fibrosis: A Review.International journal of molecular sciences · 2019
    Review
  17. Article
  18. 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

7 authors.

James T MarchCentre for Gene and Cell Therapy, School of Biological Sciences, Royal Holloway-University of London, Egham, Surrey TW20 0EX, UK. James.March.2013@live.rhul.ac.uk.
Golnoush GolshiraziCentre for Gene and Cell Therapy, School of Biological Sciences, Royal Holloway-University of London, Egham, Surrey TW20 0EX, UK. Golnoush.Golshirazi.2014@live.rhul.ac.uk.
Viktorija CernisovaCentre for Gene and Cell Therapy, School of Biological Sciences, Royal Holloway-University of London, Egham, Surrey TW20 0EX, UK. Viktorija.Cernisova.2013@live.rhul.ac.uk.
Heidi CarrCentre for Gene and Cell Therapy, School of Biological Sciences, Royal Holloway-University of London, Egham, Surrey TW20 0EX, UK. Heidi.Carr.2014@live.rhul.ac.uk.
Yee LeongCentre for Gene and Cell Therapy, School of Biological Sciences, Royal Holloway-University of London, Egham, Surrey TW20 0EX, UK. Yee.Leong.2016@live.rhul.ac.uk.
Ngoc Lu-NguyenCentre for Gene and Cell Therapy, School of Biological Sciences, Royal Holloway-University of London, Egham, Surrey TW20 0EX, UK. Ngoc.Lu-Nguyen@rhul.ac.uk.
Linda J PopplewellCentre for Gene and Cell Therapy, School of Biological Sciences, Royal Holloway-University of London, Egham, Surrey TW20 0EX, UK. Linda.Popplewell@rhul.ac.uk.ORCID 0000-0002-9417-4073

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis results from the excessive accumulation of extracellular matrix in chronically injured tissue. The fibrotic process is governed by crosstalk between many signaling pathways. The search for an effective treatment is further complicated by the fact that there is a degree of tissue-specificity in the pathways involved, although the process is not completely understood for all tissues. A plethora of drugs have shown promise in pre-clinical models, which is not always borne out translationally in clinical trial. With the recent approvals of two antisense oligonucleotides for the treatment of the genetic diseases Duchenne muscular dystrophy and spinal muscular atrophy, we explore here the potential of antisense oligonucleotides to knockdown the expression of pro-fibrotic proteins. We give an overview of the generalized fibrotic process, concentrating on key players and highlight where antisense oligonucleotides have been used effectively in cellular and animal models of different fibrotic conditions. Consideration is given to the advantages antisense oligonucleotides would have as an anti-fibrotic therapy alongside factors that would need to be addressed to improve efficacy. A prospective outlook for the development of antisense oligonucleotides to target fibrosis is outlined.

Indexed as

antisense oligonucleotidefibrosistransforming growth factor beta

Identifiers

PMID29941814
PMCPMC6164894

What OpenQuestion holds

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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.