Evidence map›Paper›PMID 28970796›Full record

ReviewFrontiers in pharmacology2017

Is There a Potential Therapeutic Role for Caveolin-1 in Fibrosis?

Waled A Shihata, Mohammad R A Putra, Jaye P F Chin-Dusting

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Curcumin in Fibrosis Treatment: A Review.Drug design, development and therapy · 2026
    Review
  7. Loss ofLife (Basel, Switzerland) · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Is MG53 a potential therapeutic target for cancer?Frontiers in endocrinology · 2023
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Proteomic Profiling Reveals Roles of Stress Response, CaAlcoholism, clinical and experimental research · 2020
    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

3 authors at 2 institutions in 1 country.

Waled A ShihataVascular Pharmacology Laboratory, Cardiovascular Disease Program, Department of Pharmacology, Biomedical Discovery Institute, Monash UniversityClayton, VIC, Australia.
Mohammad R A PutraVascular Pharmacology Laboratory, Cardiovascular Disease Program, Department of Pharmacology, Biomedical Discovery Institute, Monash UniversityClayton, VIC, Australia.
Jaye P F Chin-DustingVascular Pharmacology Laboratory, Cardiovascular Disease Program, Department of Pharmacology, Biomedical Discovery Institute, Monash UniversityClayton, VIC, Australia.
Monash University · AUBaker Heart and Diabetes Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is a process of dysfunctional wound repair, described by a failure of tissue regeneration and excessive deposition of extracellular matrix, resulting in tissue scarring and subsequent organ deterioration. There are a broad range of stimuli that may trigger, and exacerbate the process of fibrosis, which can contribute to the growing rates of morbidity and mortality. Whilst the process of fibrosis is widely described and understood, there are no current standard treatments that can reduce or reverse the process effectively, likely due to the continuing knowledge gaps surrounding the cellular mechanisms involved. Several cellular targets have been implicated in the regulation of the fibrotic process including membrane domains, ion channels and more recently mechanosensors, specifically caveolae, particularly since these latter contain various signaling components, such as members of the TGFβ and MAPK/ERK signaling pathways, all of which are key players in the process of fibrosis. This review explores the anti-fibrotic influences of the caveola, and in particular the key underpinning protein, caveolin-1, and its potential as a novel therapeutic target.

Indexed as

cardiac fibrosiscaveolaecaveolin-1kidney fibrosislung fibrosis

Identifiers

PMID28970796
PMCPMC5609631
OpenAlexW2749161757

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.