Evidence map›Paper›PMID 30674965›Full record

ArticleScientific reports2019

Discovery and evaluation of inhibitor of LARP6 as specific antifibrotic compound.

Branko Stefanovic, Zarko Manojlovic, Cynthia Vied, Crystal-Dawn Badger, Lela Stefanovic

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.6field-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

28 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. LARP6-mediated cardiomyocyte-fibroblast signaling prevents hypertension-induced cardiac dysfunction.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  7. Article
  8. Targeting collagen to optimize cancer immunotherapy.Experimental hematology & oncology · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Biomolecular NMR assignments · 2024
    Article
  14. Article
  15. SFPQ and Its Isoform as Potential Biomarker for Non-Small-Cell Lung Cancer.International journal of molecular sciences · 2023
    Article
  16. Myofibroblast specific targeting approaches to improve fibrosis treatment.Chemical communications (Cambridge, England) · 2022
    Review
  17. Review
  18. Article
  19. Article
  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 1 country.

Branko StefanovicDepartment of Biomedical Sciences, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, FL, 32306, USA. branko.stefanovic@med.fsu.edu.
Zarko ManojlovicKeck School of Medicine of University of Southern California, 1450 Biggy Street, NRT 4510, Los Angeles, CA, 90033, USA.
Cynthia ViedTranslational Science Laboratory, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, FL, 32306, USA.ORCID 0000-0003-3941-3614
Crystal-Dawn BadgerTranslational Science Laboratory, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, FL, 32306, USA.
Lela StefanovicDepartment of Biomedical Sciences, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, FL, 32306, USA.
Florida State University · USUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is characterized by excessive production of type I collagen. Biosynthesis of type I collagen in fibrosis is augmented by binding of protein LARP6 to the 5' stem-loop structure (5'SL), which is found exclusively in type I collagen mRNAs. A high throughput screen was performed to discover inhibitors of LARP6 binding to 5'SL, as potential antifibrotic drugs. The screen yielded one compound (C9) which was able to dissociate LARP6 from 5' SL RNA in vitro and to inactivate the binding of endogenous LARP6 in cells. Treatment of hepatic stellate cells (liver cells responsible for fibrosis) with nM concentrations of C9 reduced secretion of type I collagen. In precision cut liver slices, as an ex vivo model of hepatic fibrosis, C9 attenuated the profibrotic response at 1 μM. In prophylactic and therapeutic animal models of hepatic fibrosis C9 prevented development of fibrosis or hindered the progression of ongoing fibrosis when administered at 1 mg/kg. Toxicogenetics analysis revealed that only 42 liver genes changed expression after administration of C9 for 4 weeks, suggesting minimal off target effects. Based on these results, C9 represents the first LARP6 inhibitor with significant antifibrotic activity.

Indexed as

Down-RegulationAnimalsAutoantigensCells, CulturedCollagen Type IDisease Models, AnimalDrug Evaluation, PreclinicalEnzyme InhibitorsHepatic Stellate CellsHumansLiver CirrhosisModels, BiologicalRats, WistarRibonucleoproteinsSS-B AntigenTreatment OutcomeAutoantigensCollagen Type IEnzyme InhibitorsRibonucleoproteinsSS-B Antigen

Identifiers

PMID30674965
PMCPMC6344531
OpenAlexW2914411948

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.