Evidence map›Paper›PMID 25792482›Full record

ReviewExperimental neurology2015

Molecular regulators of nerve conduction - Lessons from inherited neuropathies and rodent genetic models.

Jun Li

Open access · greenAbstract readReview
In one paragraph

Review in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Basic Pathological Mechanisms in Peripheral Nerve Diseases.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Demyelination in hereditary sensory neuropathy type-1C.Annals of clinical and translational neurology · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Caveats in the Established Understanding of CMT1A.Annals of clinical and translational neurology · 2017
    Article
  20. 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

1 author at 1 institution in 1 country.

Jun LiDepartment of Neurology, Center for Human Genetic Research, Vanderbilt Brain Institute, Vanderbilt University School of Medicine, Nashville, TN, USA; Tennessee Valley Healthcare System, Nashville VA, Nashville, TN, USA. Electronic address: jun.li.2@vanderbilt.edu.
Vanderbilt University · US

Funding

Pathophysiology of Conduction Block in HNPP.R01NS066927 · NINDS · WAYNE STATE UNIVERSITY · PI LI, JUN · 2010 to 2019
$3.5M
SVIP and CMT1AR21NS081364 · NINDS · VANDERBILT UNIVERSITY · PI LI, JUN · 2012 to 2013
$348k
NINDS NIH HHS R01 NS066927NINDS NIH HHS R01NS066927NINDS NIH HHS R21 NS081364NINDS NIH HHS R21NS081364
6 · The paper itself

Abstract

Myelinated nerve fibers are highly compartmentalized. Helically wrapped lipoprotein membranes of myelin are integrated with subsets of proteins specifically in each compartment to shape the physiological behavior of these nerve fibers. With the advance of molecular biology and genetics, many functions of these proteins have been revealed over the past decade. In this review, we will first discuss how action potential propagation has been understood by classical electrophysiological studies. In particular, the discussion will be concentrated on how the geometric dimensions of myelinated nerve fibers (such as internodal length and myelin thickness) may affect nerve conduction velocity. This discussion will then extend into how specific myelin proteins may shape these geometric parameters, thereby regulating action potential propagation. For instance, periaxin may specifically affect the internodal length, but not other parameters. In contrast, neuregulin-1 may affect myelin thickness, but not axon diameter or internodal length. Finally, we will discuss how these basic neurobiological observations can be applied to inherited peripheral nerve diseases.

Indexed as

Peripheral Nervous System DiseasesAction PotentialsAnimalsDisease Models, AnimalMyelin ProteinsNerve Fibers, MyelinatedNeural ConductionRodentiaMyelin ProteinsAction potentialAdherens junctionAxonal degenerationCasprCharcot–Marie–Tooth diseaseCMT1ACMT2CMTX1Compound muscle action potentialConnexin-1DemyelinationHereditary neuropathy with liability to pressure palsiesHNPPInherited neuropathyIon channelJuxtaparanodeMyelinationNerve conduction studyNode of RanvierParanodePMP22PolyneuropathySensory nerve action potentialSeptate-like junctionTight junctionVoltage-gated potassium channelVoltage-gated sodium channel

Identifiers

PMID25792482
PMCPMC4417062
OpenAlexW2077843597

What OpenQuestion 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 OpenQuestion graph.