Evidence map›Paper›PMID 20626609›Full record

ArticleThe journal of sexual medicine2010

Hypercholesterolemia-induced erectile dysfunction: endothelial nitric oxide synthase (eNOS) uncoupling in the mouse penis by NAD(P)H oxidase.

Biljana Musicki, Tongyun Liu, Gwen A Lagoda, Travis D Strong, Sena F Sezen, Justin M Johnson, Arthur L Burnett

Abstract read
In one paragraph

Article in The journal of sexual medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 111 citations in OpenAlex.

  1. Trial
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  7. Article
  8. Erectile Dysfunction and Oxidative Stress: A Narrative Review.International journal of molecular sciences · 2025
    Review
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  10. Review
  11. Article
  12. Article
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  16. Potential Therapeutic Role of Dietary Supplementation withOxidative medicine and cellular longevity · 2020
    Article
  17. Review
  18. Article
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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

7 authors at 1 institution in 1 country.

Biljana MusickiDepartment of Urology, Johns Hopkins University, Baltimore, MD 21287, USA. bmusicki@jhmi.edu
Tongyun Liu
Gwen A Lagoda
Travis D Strong
Sena F Sezen
Justin M Johnson
Arthur L Burnett
Johns Hopkins University · US

Funding

eNOS-Protein Interaction in the PenisR21DK075782 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI MUSICKI, BILJANA · 2006 to 2007
$444k
NIDDK NIH HHS DK075782NIDDK NIH HHS R21 DK075782
6 · The paper itself

Abstract

introductionHypercholesterolemia induces erectile dysfunction (ED) mostly by increasing oxidative stress and impairing endothelial function in the penis, but the mechanisms regulating reactive oxygen species (ROS) production in the penis are not understood.

aimsWe evaluated whether hypercholesterolemia activates nicotinamide adenine dinucleotide phosphate (NAD[P]H) oxidase in the penis, providing an initial source of ROS to induce endothelial nitric oxide synthase (eNOS) uncoupling and endothelial dysfunction resulting in ED.

methodsLow-density-lipoprotein receptor (LDLR)-null mice were fed Western diet for 4 weeks to induce early-stage hyperlipidemia. Wild type (WT) mice fed regular chow served as controls. Mice received NAD(P)H oxidase inhibitor apocynin (10 mM in drinking water) or vehicle. Erectile function was assessed in response to cavernous nerve electrical stimulation. Markers of endothelial function (phospho [P]-vasodilator-stimulated-protein [VASP]-Ser-239), oxidative stress (4-hydroxy-2-nonenal [HNE]), sources of ROS (eNOS uncoupling and NAD[P]H oxidase subunits p67(phox) , p47(phox) , and gp91(phox) ), P-eNOS-Ser-1177, and eNOS were measured by Western blot in penes.

main outcome measuresThe main outcome measures are the molecular mechanisms of ROS generation and endothelial dysfunction in hypercholesterolemia-induced ED.

resultsErectile response was significantly (P<0.05) reduced in hypercholesterolemic LDLR-null mice compared with WT mice. Relative to WT mice, hypercholesterolemia increased (P<0.05) protein expressions of NAD(P)H oxidase subunits p67(phox) , p47(phox) and gp91(phox) , eNOS uncoupling, and 4-HNE-modified proteins, and reduced (P<0.05) P-VASP-Ser-239 expression in the penis. Apocynin treatment of LDLR-null mice preserved (P<0.05) maximal intracavernosal pressure, and reversed (P<0.05) the abnormalities in protein expressions of gp67(phox) and gp47(phox) , 4-HNE, P-VASP-Ser-239, and eNOS uncoupling in the penis. Apocynin treatment of WT mice did not affect any of these parameters. Protein expressions of P-eNOS-Ser-1177 and total eNOS were unaffected by hypercholesterolemia.

conclusionActivated NAD(P)H oxidase in the penis is an initial source of oxidative stress resulting in eNOS uncoupling, thus providing a mechanism of eNOS uncoupling and endothelial dysfunction in hypercholesterolemia-induced ED.

Indexed as

AcetophenonesAldehydesAnimalsCell Adhesion MoleculesCholesterol, DietaryDisease Models, AnimalEndothelium, VascularEnzyme InhibitorsErectile DysfunctionHypercholesterolemiaMaleMiceMicrofilament ProteinsNADPH OxidasesNitric Oxide Synthase Type IIIPenis4-hydroxy-2-nonenalAcetophenonesacetovanilloneAldehydesCell Adhesion MoleculesCholesterol, DietaryEnzyme InhibitorsMicrofilament ProteinsNADPH OxidasesNitric Oxide Synthase Type IIINos3 protein, mousePhosphoproteinsReactive Oxygen SpeciesVasodilator-Stimulated Phosphoprotein

Identifiers

PMID20626609
PMCPMC2958216
OpenAlexW2124559568

What OpenQuestion holds

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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.