Evidence map›Paper›PMID 29486776›Full record

ArticleMolecular brain2018

TLR4-mediated autophagic impairment contributes to neuropathic pain in chronic constriction injury mice.

Yibo Piao, Do Hyeong Gwon, Dong-Wook Kang, Tae Woong Hwang, Nara Shin, Hyeok Hee Kwon, Hyo Jung Shin, Yuhua Yin, Jwa-Jin Kim, Jinpyo Hong and 5 more

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-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

30 citing papers in PubMed, 46 citations in OpenAlex.

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  13. Intrathecal Administration of an Anti-nociceptive Non-CpG Oligodeoxynucleotide Reduces Glial Activation and Central Sensitization.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021
    Article
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  18. Strategies for Biomaterial-Based Spinal Cord Injury RepairFrontiers in bioengineering and biotechnology · 2021
    Review
  19. 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

15 authors at 4 institutions in 2 countries.

Yibo PiaoDepartment of Plastic and Reconstructive Surgery, Department of Pediatrics, Department of Anesthesiology and Pain Medicine, Chungnam National University Hospital, Daejeon, 35015, Republic of Korea.
Do Hyeong GwonDepartment of Medical Science, Department of Physiology, Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Dong-Wook KangDepartment of Medical Science, Department of Physiology, Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Tae Woong HwangDepartment of Medical Science, Department of Physiology, Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Nara ShinDepartment of Plastic and Reconstructive Surgery, Department of Pediatrics, Department of Anesthesiology and Pain Medicine, Chungnam National University Hospital, Daejeon, 35015, Republic of Korea.
Hyeok Hee KwonDepartment of Plastic and Reconstructive Surgery, Department of Pediatrics, Department of Anesthesiology and Pain Medicine, Chungnam National University Hospital, Daejeon, 35015, Republic of Korea.
Hyo Jung ShinDepartment of Medical Science, Department of Physiology, Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Yuhua YinDepartment of Plastic and Reconstructive Surgery, Department of Pediatrics, Department of Anesthesiology and Pain Medicine, Chungnam National University Hospital, Daejeon, 35015, Republic of Korea.
Jwa-Jin KimDepartment of Medical Science, Department of Physiology, Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Jinpyo HongDepartment of Medical Science, Department of Physiology, Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Hyun-Woo KimDepartment of Medical Science, Department of Physiology, Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea.
Yonghyun KimDepartment of Chemical and Biological Engineering, The University of Alabama, Tuscaloosa, AL, 35487, USA.
Sang Ryong KimSchool of Life Sciences, BK21 plus KNU Creative BioResearch Group, Institute of Life Science & Biotechnology, Kyungpook National University, Daegu, 41566, South Korea.
Sang-Ha OhDepartment of Plastic and Reconstructive Surgery, Department of Pediatrics, Department of Anesthesiology and Pain Medicine, Chungnam National University Hospital, Daejeon, 35015, Republic of Korea. djplastic@cnu.ac.kr.
Dong Woon KimDepartment of Medical Science, Department of Physiology, Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 35015, Republic of Korea. visnu528@cnu.ac.kr.ORCID 0000-0001-7691-1394
Chungnam National University · KRChungnam National University Hospital · KRKyungpook National University · KRUniversity of Alabama · US

Funding

Ministry of Science, ICT and Future Planning 2013R1A1A1057928Ministry of Science, ICT and Future Planning 2016R1A2B4009409Ministry of Science, ICT and Future Planning 2017R1D1A1B03028839National Research Foundation of Korea NRF-2016M3C7A1905074
6 · The paper itself

Abstract

Neuropathic pain is a complex, chronic pain state characterized by hyperalgesia, allodynia, and spontaneous pain. Accumulating evidence has indicated that the microglial Toll-like receptor 4 (TLR4) and autophagy are implicated in neurodegenerative diseases, but their relationship and role in neuropathic pain remain unclear. In this study, we examined TLR4 and its association with autophagic activity using a chronic constriction injury (CCI)-induced neuropathic pain model in wild-type (WT) and TLR4-knockout (KO) mice. The mice were assigned into four groups: WT-Contralateral (Contra), WT-Ipsilateral (Ipsi), TLR4 KO-Contra, and TLR4 KO-Ipsi. Behavioral and mechanical allodynia tests and biochemical analysis of spinal cord tissue were conducted following CCI to the sciatic nerve. Compared with the Contra group, mechanical allodynia in both the WT- and TLR4 KO-Ipsi groups was significantly increased, and a marked decrease of allodynia was observed in the TLR4 KO-Ipsi group. Although glial cells were upregulated in the WT-Ipsi group, no significant change was observed in the TLR4 KO groups. Moreover, protein expression and immunoreactive cell regulation of autophagy (Beclin 1, p62) were significantly increased in the neurons, but not microglia, of WT-Ipsi group compared with the WT-Contra group. The level of PINK1, a marker for mitophagy was increased in the neurons of WT, but not in TLR4 KO mice. Together, these results show that TLR4-mediated p62 autophagic impairment plays an important role in the occurrence and development of neuropathic pain. And what is more, microglial TLR4-mediated microglial activation might be indirectly coupled to neuronal autophage.

Indexed as

AutophagyAnimalsAstrocytesBeclin-1Chronic DiseaseConstrictionHyperalgesiaMaleMice, Inbred C57BLMice, KnockoutMicrogliaMicrotubule-Associated ProteinsMitophagyModels, NeurologicalNeuralgiaNociceptionBeclin-1Becn1 protein, mouseMap1lc3b protein, mouseMicrotubule-Associated ProteinsProtein KinasesPTEN-Induced Putative KinaseSequestosome-1 ProteinSqstm1 protein, mouseTlr4 protein, mouseToll-Like Receptor 4AutophagyCCIGliaNeuropathic painTLR4

Identifiers

PMID29486776
PMCPMC5830083
OpenAlexW2795369734

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.