Evidence map›Paper›PMID 36238284›Full record

ArticleFrontiers in immunology2022

Cannabinoid receptor-2 attenuates neuroinflammation by promoting autophagy-mediated degradation of the NLRP3 inflammasome post spinal cord injury.

Fan Jiang, Mingjie Xia, Yanan Zhang, Jie Chang, Jiang Cao, Zhongkai Zhang, Zhanyang Qian, Lei Yang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. The neuroimmune-glutamate hypothesis of addiction.Neuroscience and biobehavioral reviews · 2026
    Review
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  20. Microglia and programmed cell death in spinal cord injury: beyond apoptosis.Frontiers in cell and developmental biology · 2025
    Review
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 5 institutions in 1 country.

Fan JiangDepartment of Orthopedics, Taizhou People's Hospital, Nanjing Medical University, Taizhou, China.
Mingjie XiaDepartment of Orthopedics, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Yanan ZhangDepartment of Orthopedics, Taizhou People's Hospital, Nanjing Medical University, Taizhou, China.
Jie ChangDepartment of Orthopedics, Affiliated First Hospital of Nanjing Medical University, Nanjing, China.
Jiang CaoDepartment of Orthopedics, Affiliated First Hospital of Nanjing Medical University, Nanjing, China.
Zhongkai ZhangDepartment of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Zhanyang QianDepartment of Orthopedics, Zhongda Hospital, Nanjing, China.
Lei YangDepartment of Orthopedics, Taizhou People's Hospital, Nanjing Medical University, Taizhou, China.
Nanjing Medical University · CNNantong University · CNShandong First Medical University · CNTaizhou People's Hospital · CNZhongda Hospital Southeast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Neuroinflammation following spinal cord injury (SCI) results in prolonged neurological damage and locomotor dysfunction. Polarization of microglia is vital to regulation of neuroinflammation, although the underlying mechanisms have not yet been elucidated. Endocannabinoid receptor subtype 2 (CB2R) is reported to ameliorate neurodegeneration Methods: A lipopolysaccharide-induced microglia inflammation model and a mouse model of SCI were employed to investigate the regulatory role of CB2R in the polarization of microglia in response to excess neuroinflammation. Markers of inflammation and autophagy were measured by Western blot analysis, immunofluorescence, flow cytometry, and enzyme-linked immunosorbent assays. Histological staining with hematoxylin and eosin, Nissl, and Luxol Results: The results showed that CB2R promoted M2 differentiation, increased interleukin (IL)-10 expression, and inhibited M1 differentiation with decreased expression of IL-1β and IL-6. CB2R activation also increased ubiquitination of the NLRP3 inflammasome and interacted with the autophagy-related proteins p62 and microtubule-associated proteins 1B light chain 3. Treatment with the CB2R activator JWH-133 reduced loss of myelin, apoptosis of neurons, and glial scarring, leading to improved functional recovery of the hindlimbs, while the CB2R antagonist AM630 produced opposite results. Conclusion: Taken together, these results suggested that CB2R activation attenuated neuroinflammation targeting microglial polarization by promoting NLRP3 clearance, thereby facilitating functional recovery post-SCI.

Indexed as

InflammasomesSpinal Cord InjuriesAnimalsAutophagyAutophagy-Related ProteinsEndocannabinoidsEosine Yellowish-(YS)HematoxylinInflammationInterleukin-6LipopolysaccharidesMiceMicrotubule-Associated ProteinsNeuroinflammatory DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinReceptors, CannabinoidAutophagy-Related ProteinsEndocannabinoidsEosine Yellowish-(YS)HematoxylinInflammasomesInterleukin-6LipopolysaccharidesMicrotubule-Associated ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReceptors, Cannabinoidautophagycannabinoid receptor-2neuroinflammationNLRP3spinal cord injury

Identifiers

PMID36238284
PMCPMC9553321
OpenAlexW4297371828

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.