Evidence map›Paper›PMID 11426341›Full record

ReviewInternational journal of impotence research2001

RhoA/Rho-kinase: a novel player in the regulation of penile erection.

K Chitaley, R C Webb, T M Mills

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of impotence research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
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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.

K ChitaleyDepartment of Physiology, University of Michigan, Ann Arbor, MI, USA. kanchanc@umich.edu
R C Webb
T M Mills

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current research has centered around the role of nitric oxide in the stimulation of cavernosal vasodilation and erection. However, recent evidence from our lab details the importance of endogenous vasoconstrictor mechanisms in maintaining a flaccid penile state, and further demonstrates that the inhibition of endogenous vasoconstriction is sufficient to stimulate erection in a rat model. In this article, we suggest inhibition of endogenous vasoconstriction as a potential therapeutic avenue in the treatment of erectile dysfunction. We also speculate on potential physiologic mechanisms by which endogenous vasoconstriction is inhibited in order for arousal-initiated vasorelaxation, and erection, to occur.

Indexed as

Enzyme InhibitorsErectile DysfunctionHumansIntracellular Signaling Peptides and ProteinsMalePenile ErectionPenisProtein Serine-Threonine KinasesrhoA GTP-Binding Proteinrho-Associated KinasesVasoconstrictionVasodilationEnzyme InhibitorsIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesrhoA GTP-Binding Proteinrho-Associated Kinases

Identifiers

PMID11426341

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.