Evidence map›Paper›PMID 25645145›Full record

ArticleMolecular pain2015

Spinal autophagy is differently modulated in distinct mouse models of neuropathic pain.

Laura Berliocchi, Maria Maiarù, Giuseppe Pasquale Varano, Rossella Russo, Maria Tiziana Corasaniti, Giacinto Bagetta, Cristina Tassorelli

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 66 citations in OpenAlex.

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  13. The Role of Autophagy and Apoptosis in Neuropathic Pain Formation.International journal of molecular sciences · 2022
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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

7 authors at 3 institutions in 1 country.

Laura BerliocchiDepartment of Health Sciences, University "Magna Græcia" of Catanzaro, 88100, Catanzaro, Italy. berliocchi@unicz.it.
Maria MaiarùDepartment of Pharmacy, Health and Nutritional Sciences, Section of Preclinical and Translational Pharmacology, University of Calabria, 87036, Rende, Cosenza, Italy. mariamaiaru@hotmail.it.
Giuseppe Pasquale VaranoC. Mondino National Neurological Institute, Pavia, Italy. giuseppe.varano@hotmail.it.
Rossella RussoDepartment of Pharmacy, Health and Nutritional Sciences, Section of Preclinical and Translational Pharmacology, University of Calabria, 87036, Rende, Cosenza, Italy. rossella.russo@unical.it.
Maria Tiziana CorasanitiDepartment of Health Sciences, University "Magna Græcia" of Catanzaro, 88100, Catanzaro, Italy. mtcorasa@unicz.it.
Giacinto BagettaCentre of Neuropharmacology of Normal and Pathological Synaptic Plasticity, University Consortium for Adaptive Disorders and Head Pain, 87036, Rende, Cosenza, Italy. g.bagetta@unical.it.
Cristina TassorelliC. Mondino National Neurological Institute, Pavia, Italy. cristina.tassorelli@mondino.it.
University of Calabria · ITFondazione Istituto Neurologico Nazionale Casimiro Mondino · ITMagna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutophagy is a homeostatic degradative process essential for basal turnover of long-lived proteins and organelles as well as for removal of dysfunctional cellular components. Dysregulation of the autophagic machinery has been recently associated to several conditions including neurodegenerative diseases and cancer, but only very few studies have investigated its role in pain processing.

resultsWe previously described autophagy impairment at the spinal cord in the experimental model of neuropathic pain induced by spinal nerve ligation (SNL). In this study, we characterized the main autophagic markers in two other common experimental models of neuropathic pain, the chronic constriction injury (CCI) and the spared nerve injury (SNI). The different modulation of LC3-I, Beclin 1 and p62 suggested that autophagy is differentially affected in the spinal dorsal horn depending on the type of peripheral injury. Confocal analysis of p62 distribution in the spinal dorsal horn indicated its presence mainly in NeuN-positive cell bodies and occasionally in glial processes, thus suggesting a predominant expression in the neuronal compartment. Finally, we investigated the consequences of autophagy impairment on pain behaviour by using the autophagy blocker cloroquine. Intrathecal chloroquine injection in naïve mice induced spinal accumulation of LC3 and p62 paralleled by significant mechanical hypersensitivity thus confirming the block in autophagosome clearance and suggesting the participation of the autophagic process in spinal mechanisms of pain processing. Altogether, our data indicate that spinal autophagy is differentially altered in different experimental pain models of neuropathic pain and that this process may be relevant for pain control.

Indexed as

AutophagyAdaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsBeclin-1Behavior, AnimalBiomarkersBlotting, WesternChloroquineDensitometryHeat-Shock ProteinsHyperalgesiaInjections, SpinalLigationMaleMice, Inbred C57BLAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBeclin-1Becn1 protein, mouseBiomarkersChloroquineHeat-Shock ProteinsMap1lc3b protein, mouseMicrotubule-Associated ProteinsSequestosome-1 ProteinSqstm1 protein, mouse

Identifiers

PMID25645145
PMCPMC4417307
OpenAlexW2096867586

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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.