Evidence map›Paper›PMID 21995851›Full record

ArticleThe journal of sexual medicine2011

FK506 neuroprotection after cavernous nerve injury is mediated by thioredoxin and glutathione redox systems.

Gwen Lagoda, Yi Xie, Sena F Sezen, K Joseph Hurt, Limin Liu, Biljana Musicki, Arthur L Burnett

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in The journal of sexual medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The neurochemistry of peripheral nerve regeneration.Indian journal of plastic surgery : official publication of the Association of Plastic Surgeons of India
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Gwen LagodaDepartment of Urology, The James Buchanan Brady Urological Institute, The Johns Hopkins Hospital and The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Yi Xie
Sena F Sezen
K Joseph Hurt
Limin Liu
Biljana Musicki
Arthur L Burnett
Johns Hopkins University · USJohns Hopkins Hospital · USChongqing Public Health Medical Center · CNUniversity of California, San Francisco · US

Funding

NOS Regulation in the PenisR01DK067223 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI BURNETT, ARTHUR LOUIS · 2005 to 2015
$3.5M
NIDDK NIH HHS R01 DK067223
6 · The paper itself

Abstract

introductionImmunophilin ligands such as FK506 (FK) preserve erectile function (EF) following cavernous nerve injury (CNI), although the precise mechanisms are unclear. We examined whether the thioredoxin (Trx) and glutathione (GSH) redox systems mediate this effect after CNI.

aimTo investigate the roles of Trx reductase 2 (TrxR2) and S-Nitrosoglutathione reductase (GSNOR) as antioxidative/nitrosative and antiapoptotic mediators of the neuroprotective effect of FK in the penis after CNI.

methodsAdult male rats, wild-type (WT) mice, and GSNOR deficient (GSNOR -/-) mice were divided into four groups: sham surgery (CN [cavernous nerves] exposure only) + vehicle; sham surgery + FK (5 mg/kg/day/rat or 2 mg/kg/day/mouse, for 2 days, subcutaneous); CNI + vehicle; and CNI + FK. At day 4 after injury, electrically stimulated changes in intracavernosal pressure (ICP) were measured. Penises were collected for Western blot analysis of TrxR2, GSNOR, and Bcl-2, and for immunolocalization of TrxR2 and GSNOR.

main outcome measuresEF assessment represented by maximal ICP and total ICP in response to electrical stimulation. Evaluation of protein expression levels and distribution patterns of antioxidative/nitrosative and antiapoptotic factors in penile tissue.

resultsEF decreased after CNI compared with sham surgery values in both rats (P < 0.01) and WT and GSNOR -/- mice (P < 0.05). FK treatment preserved EF after CNI compared with vehicle treatment in rats (P < 0.01) and WT mice (P < 0.05) but not in GSNOR -/- mice. In rats, GSNOR (P < 0.01) and Bcl-2 (P < 0.05) expressions were significantly decreased after CNI. FK treatment in CN-injured rats restored expression of GSNOR and upregulated TrxR2 (P < 0.001) and Bcl-2 (P < 0.001) expressions compared with vehicle treatment. Localizations of proteins in the penis were observed for TrxR2 (endothelium, smooth muscle) and for GSNOR (nerves, endothelium, smooth muscle).

conclusionsThe neuroprotective effect of FK in preserving EF after CNI involves antioxidative/nitrosative and antiapoptotic mechanisms mediated, to some extent, by Trx and GSH systems.

Indexed as

Aldehyde OxidoreductasesAnimalsApoptosisDisease Models, AnimalGlutathioneImmunosuppressive AgentsMaleNeuroprotective AgentsOxidation-ReductionOxidative StressPenisProstaglandinsRatsRats, Sprague-DawleyStatistics as TopicTacrolimusAldehyde Oxidoreductasesformaldehyde dehydrogenase, glutathione-independentGlutathioneImmunosuppressive AgentsNeuroprotective AgentsProstaglandinsTacrolimusThioredoxin Reductase 2ThioredoxinsTXNRD2 protein, human

Identifiers

PMID21995851
PMCPMC4479158
OpenAlexW1885851658

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.