Evidence map›Paper›PMID 25945352›Full record

ArticleJournal of diabetes research2015

Therapeutic Benefit of Extended Thymosin β4 Treatment Is Independent of Blood Glucose Level in Mice with Diabetic Peripheral Neuropathy.

Lei Wang, Michael Chopp, Longfei Jia, Xuerong Lu, Alexandra Szalad, Yi Zhang, RuiLan Zhang, Zheng Gang Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

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  11. Tβ4-Ac-SDKP pathway: Any relevance for the cardiovascular system?Canadian journal of physiology and pharmacology · 2019
    Review
  12. Tubule-vascular feedback in renal autoregulation.American journal of physiology. Renal physiology · 2019
    Review
  13. Article
  14. Review
  15. Article
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  18. Article
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 2 institutions in 1 country.

Lei WangDepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USA.
Michael ChoppDepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USA ; Department of Physics, Oakland University, Rochester, MI 48309, USA.
Longfei JiaDepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USA.
Xuerong LuDepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USA.
Alexandra SzaladDepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USA.
Yi ZhangDepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USA.
RuiLan ZhangDepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USA.
Zheng Gang ZhangDepartment of Neurology, Henry Ford Hospital, 2799 W. Grand Boulevard, Detroit, MI 48202, USA.
Henry Ford Hospital · USOakland University · US

Funding

MicroRNAs and neurogenesis after strokeR01NS075156 · NINDS · HENRY FORD HEALTH SYSTEM · PI ZHANG, ZHENG GANG · 2011 to 2015
$1.6M
MSCs Induce Brain Plasticity via tPAR01AG037506 · NIA · HENRY FORD HEALTH SYSTEM · PI CHOPP, MICHAEL · 2011 to 2015
$1.5M
Thymosin Beta4 Promotes the Recovery of Peripheral neuropathy in Type II DiabeticR01DK097519 · NIDDK · HENRY FORD HEALTH SYSTEM · PI WANG, LEI · 2013 to 2016
$1.3M
PDE5 is a Therapeutic Target for Peripheral Neuropathy in Diabetic MiceR01NS075084 · NINDS · HENRY FORD HEALTH SYSTEM · PI WANG, LEI · 2012 to 2015
$1.3M
NIA NIH HHS R01 AG037506NIDDK NIH HHS R01 DK097519NINDS NIH HHS R01 NS075084NINDS NIH HHS R01 NS075156
6 · The paper itself

Abstract

Peripheral neuropathy is a chronic complication of diabetes mellitus. To investigated the efficacy and safety of the extended treatment of diabetic peripheral neuropathy with thymosin β4 (Tβ4), male diabetic mice (db/db) at the age of 24 weeks were treated with Tβ4 or saline for 16 consecutive weeks. Treatment of diabetic mice with Tβ4 significantly improved motor (MCV) and sensory (SCV) conduction velocity in the sciatic nerve and the thermal and mechanical latency. However, Tβ4 treatment did not significantly alter blood glucose levels. Treatment with Tβ4 significantly increased intraepidermal nerve fiber density. Furthermore, Tβ4 counteracted the diabetes-induced axon diameter and myelin thickness reductions and the g-ratio increase in sciatic nerve. In vitro, compared with dorsal root ganglia (DRG) neurons derived from nondiabetic mice, DRG neurons derived from diabetic mice exhibited significantly decreased neurite outgrowth, whereas Tβ4 promoted neurite growth in these diabetic DRG neurons. Blockage of the Ang1/Tie2 signaling pathway with a neutralized antibody against Tie2 abolished Tβ4-increased neurite outgrowth. Our data demonstrate that extended Tβ4 treatment ameliorates diabetic-induced axonal degeneration and demyelination, which likely contribute to therapeutic effect of Tβ4 on diabetic neuropathy. The Ang1/Tie2 pathway may mediate Tβ4-induced axonal remodeling.

Indexed as

AnimalsBlood GlucoseDiabetes Mellitus, Type 2Diabetic NeuropathiesDisease Models, AnimalGanglia, SpinalMaleMiceNerve FibersSciatic NerveSignal TransductionThymosinThymosin beta(4)Treatment OutcomeBlood GlucoseThymosinThymosin beta(4)

Identifiers

PMID25945352
PMCPMC4405294
OpenAlexW2049245068

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.