Evidence map›Paper›PMID 17967455›Full record

ArticleExperimental neurology2008

Erythropoietin and its carbamylated derivative prevent the development of experimental diabetic autonomic neuropathy in STZ-induced diabetic NOD-SCID mice.

Robert E Schmidt, Karen G Green, Dongyan Feng, Denise A Dorsey, Curtis A Parvin, Jin-Moo Lee, Qinlgi Xiao, Michael Brines

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  9. Erythropoietin: still on the neuroprotection road.Therapeutic advances in neurological disorders · 2012
    Article
  10. Article
  11. Article
  12. Prevention of diabetic neuropathy by regulatable expression of HSV-mediated erythropoietin.Molecular therapy : the journal of the American Society of Gene Therapy · 2011
    Article
  13. Article
  14. Schwann cells as a therapeutic target for peripheral neuropathies.CNS & neurological disorders drug targets · 2010
    Review
  15. Article
  16. Article
  17. Therapeutic potential of erythropoietin and its structural or functional variants in the nervous system.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2009
    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

8 authors at 1 institution in 1 country.

Robert E SchmidtDepartment of Pathology and Immunology, Division of Neuropathology, Washington University School of Medicine, Saint Louis, MO 63110, USA. reschmidt@wustl.edu
Karen G Green
Dongyan Feng
Denise A Dorsey
Curtis A Parvin
Jin-Moo Lee
Qinlgi Xiao
Michael Brines
Washington University in St. Louis · US

Funding

EXPERIMENTAL DIABETIC AUTONOMIC NEUROPATHYR37DK019645 · NIDDK · WASHINGTON UNIVERSITY · PI SCHMIDT, ROBERT EDWARD · 1999 to 2004
$1.6M
NIDDK NIH HHS R37 DK019645
6 · The paper itself

Abstract

Autonomic neuropathy is a significant diabetic complication resulting in increased morbidity and mortality. Studies of autopsied diabetic patients and several rodent models demonstrate that the neuropathologic hallmark of diabetic sympathetic autonomic neuropathy in prevertebral ganglia is the occurrence of synaptic pathology resulting in distinctive dystrophic neurites ("neuritic dystrophy"). Our prior studies show that neuritic dystrophy is reversed by exogenous IGF-I administration without altering the metabolic severity of diabetes, i.e. functioning as a neurotrophic substance. The description of erythropoietin (EPO) synergy with IGF-I function and the recent discovery of EPO's multifaceted neuroprotective role suggested it might substitute for IGF-I in treatment of diabetic autonomic neuropathy. Our current studies demonstrate EPO receptor (EPO-R) mRNA in a cDNA set prepared from NGF-maintained rat sympathetic neuron cultures which decreased with NGF deprivation, a result which demonstrates clearly that sympathetic neurons express EPO-R, a result confirmed by immunohistochemistry. Treatment of STZ-diabetic NOD-SCID mice have demonstrated a dramatic preventative effect of EPO and carbamylated EPO (CEPO, which is neuroprotective but not hematopoietic) on the development of neuritic dystrophy. Neither EPO nor CEPO had a demonstrable effect on the metabolic severity of diabetes. Our results coupled with reported salutary effects of EPO on postural hypotension in a few clinical studies of EPO-treated anemic diabetic and non-diabetic patients may reflect a primary neurotrophic effect of EPO on the sympathetic autonomic nervous system, rather than a primary hematopoietic effect. These findings may represent a major clinical advance since EPO has been widely and safely used in anemic patients due to a variety of clinical conditions.

Indexed as

AnimalsCarbamatesCells, CulturedDiabetes Mellitus, ExperimentalDiabetic NeuropathiesErythropoietinGanglia, SympatheticImmunohistochemistryMaleMiceMice, Inbred NODMice, SCIDNeuritesReceptors, ErythropoietinRecombinant ProteinsReverse Transcriptase Polymerase Chain ReactionCarbamatesErythropoietinReceptors, ErythropoietinRecombinant ProteinsRNA, Messenger

Identifiers

PMID17967455
PMCPMC2233795
OpenAlexW2089321134

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.