Evidence map›Paper›PMID 22350947›Full record

ReviewCell and tissue research2012

Small-molecule-induced Rho-inhibition: NSAIDs after spinal cord injury.

M A Kopp, T Liebscher, A Niedeggen, S Laufer, B Brommer, G J Jungehulsing, S M Strittmatter, U Dirnagl, J M Schwab

Abstract readReview
In one paragraph

Review in Cell and tissue research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.

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  5. Disruption of G3BP1 granules promotes mammalian CNS and PNS axon regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

9 authors at 4 institutions in 2 countries.

M A KoppDepartment of Neurology and Experimental Neurology, Spinal Cord Injury Research, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany.
T Liebscher
A Niedeggen
S Laufer
B Brommer
G J Jungehulsing
S M Strittmatter
U Dirnagl
J M Schwab
Charité - Universitätsmedizin Berlin · DEDiagnostic and Treatment Centre Berlin · DEUniversity of Tübingen · DEYale University · US

Funding

Cortical Plasticity during Recovery from Spinal Cord InjuryR01NS080388 · NINDS · YALE UNIVERSITY · PI STRITTMATTER, STEPHEN M · 2012 to 2016
$1.8M
NINDS NIH HHS R01 NS080388
6 · The paper itself

Abstract

Limited axonal plasticity within the central nervous system (CNS) is a major restriction for functional recovery after CNS injury. The small GTPase RhoA is a key molecule of the converging downstream cascade that leads to the inhibition of axonal re-growth. The Rho-pathway integrates growth inhibitory signals derived from extracellular cues, such as chondroitin sulfate proteoglycans, Nogo-A, myelin-associated glycoprotein, oligodendrocyte-myelin glycoprotein, Ephrins and repulsive guidance molecule-A, into the damaged axon. Consequently, the activation of RhoA results in growth cone collapse and finally outgrowth failure. In turn, the inhibition of RhoA-activation blinds the injured axon to its growth inhibitory environment resulting in enhanced axonal sprouting and plasticity. This has been demonstrated in various CNS-injury models for direct RhoA-inhibition and for downstream/upstream blockade of the RhoA-associated pathway. In addition, RhoA-inhibition reduces apoptotic cell death and secondary damage and improves locomotor recovery in clinically relevant models after experimental spinal cord injury (SCI). Unexpectedly, a subset of "small molecules" from the group of non-steroid anti-inflammatory drugs, particularly the FDA-approved ibuprofen, has recently been identified as (1) inhibiting RhoA-activation, (2) enhancing axonal sprouting/regeneration, (3) protecting "tissue at risk" (neuroprotection) and (4) improving motor recovery confined to realistic therapeutical time-frames in clinically relevant SCI models. Here, we survey the effect of small-molecule-induced RhoA-inhibition on axonal plasticity and neurofunctional outcome in CNS injury paradigms. Furthermore, we discuss the body of preclinical evidence for a possible clinical translation with a focus on ibuprofen and illustrate putative risks and benefits for the treatment of acute SCI.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalHumansNeuronal Plasticityrho GTP-Binding ProteinsSignal TransductionSmall Molecule LibrariesSpinal Cord InjuriesAnti-Inflammatory Agents, Non-Steroidalrho GTP-Binding ProteinsSmall Molecule Libraries

Identifiers

PMID22350947
PMCPMC3744771
OpenAlexW1983350593

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.