Evidence map›Paper›PMID 20212516›Full record

ReviewNature reviews. Urology2010

Treatment of Peyronie's disease with PDE5 inhibitors: an antifibrotic strategy.

Nestor F Gonzalez-Cadavid, Jacob Rajfer

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Urology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 87 citations in OpenAlex.

  1. Trial
  2. Review
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  11. Review
  12. Article
  13. Review
  14. Nonsurgical management of Peyronie's disease.Nature reviews. Urology · 2019
    Review
  15. Review
  16. Review
  17. Article
  18. THE SCIENCE AND PRACTICE OF ERECTION PHYSIOLOGY: STORY OF A REVOLUTIONARY GASEOUS MOLECULE.Transactions of the American Clinical and Climatological Association · 2019
    Review
  19. Review
  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

2 authors at 2 institutions in 1 country.

Nestor F Gonzalez-CadavidDepartment of Urology, David Geffen School of Medicine at UCLA, and Los Angeles Biomedical Research Institute (LABioMed) at Harbor-UCLA Medical Center, Building F-6, 1124 West Carson Street, Torrance, CA 90502, USA. smitshaun@msn.com
Jacob Rajfer
Harbor–UCLA Medical Center · USUCLA Medical Center · US

Funding

RESEARCH INFORMATICS COREG12RR003026 · NCRR · CHARLES R. DREW UNIVERSITY OF MED &SCI · PI BAKER, RICHARD S. · 1986 to 2004
$11.5M
ERECTILE DYSFUNCTION AND NITRIC OXIDE SYNTHASE IN AGINGR01DK053069 · NIDDK · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI GONZALEZ-CADAVID, NESTOR F · 1999 to 2006
$1.6M
CELL-SELECTIVE EXPRESSION OF FIBROTIC GENE PATHWAYSR21DK070003 · NIDDK · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI GONZALEZ-CADAVID, NESTOR F · 2007 to 2008
$390k
NCRR NIH HHS G12RR-03026NIDDK NIH HHS R01DK-53069NIDDK NIH HHS R21DK-070003
6 · The paper itself

Abstract

Peyronie's disease (PD) is a localized fibrotic condition of the tunica albuginea that is associated with risk factors for corpora cavernosa fibrosis (such as advanced age and diabetes) and Dupuytren contracture, another localized fibrotic process. Most of the current pharmacological treatments for PD are not based on antifibrotic approaches that have shown promising results in animal models and clinical efficacy in other fibrotic conditions, which may explain why they are generally unsuccessful. Evidence gathered in human specimens and animal models of PD have elucidated aspects of its etiology and histopathology, showing that overexpression of transforming growth factor beta1, plasminogen activator inhibitor 1, reactive oxygen species and other profibrotic factors, which are, in most cases, assumed to be induced by trauma to the tunica albuginea, leads to myofibroblast accumulation and excessive deposition of collagen. At the same time, a steady overexpression of inducible nitric oxide synthase, leading to increased nitric oxide and cGMP levels, seems to act as an endogenous antifibrotic mechanism. This process has also been reported in corporal and cardiovascular fibrosis, and has led to the demonstration that long-term continuous administration of phosphodiesterase type 5 inhibitors counteracts the development of a PD-like fibrotic plaque in a rat model, and later extended to the prevention of corporal fibrosis in animal models of erectile dysfunction.

Indexed as

AnimalsCyclic Nucleotide Phosphodiesterases, Type 5FibrosisHumansMalePenile IndurationPenisPhosphodiesterase InhibitorsSignal TransductionTreatment OutcomeCyclic Nucleotide Phosphodiesterases, Type 5Phosphodiesterase Inhibitors

Identifiers

PMID20212516
OpenAlexW2042270638

What OpenQuestion holds

Textmetadata
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.