Evidence map›Paper›PMID 33858422›Full record

ArticleJournal of neuroinflammation2021

Orthopedic surgery-induced cognitive dysfunction is mediated by CX3CL1/R1 signaling.

Inja Cho, Jeong Min Kim, Eun Jung Kim, So Yeon Kim, Eun Hee Kam, Eunji Cheong, Minah Suh, Bon-Nyeo Koo

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Inja ChoDepartment of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, 50-1, Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Jeong Min KimDepartment of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, 50-1, Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Eun Jung KimDepartment of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, 50-1, Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
So Yeon KimDepartment of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, 50-1, Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Eun Hee KamDepartment of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, 50-1, Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.
Eunji CheongDepartment of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, Republic of Korea.
Minah SuhDepartment of Biomedical Engineering, Sungkyunkwan University, 2066, Seobu-ro, Jangan-gu, Suwon-si, Gyeong gi-do, 16419, Republic of Korea.
Bon-Nyeo KooDepartment of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, 50-1, Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea. koobn@yuhs.ac.
Yonsei University · KRSungkyunkwan University · KR

Funding

National Research Foundation of Korea 2017R1A2B4009478National Research Foundation of Korea 2020R1A2C1012017
6 · The paper itself

Abstract

backgroundPostoperative pain is a common phenomenon after surgery and is closely associated with the development of postoperative cognitive dysfunction (POCD). Persistent pain and systemic inflammation caused by surgery have been suggested as key factors for the development of POCD. Fractalkine (CX3CL1) and its receptor, the CX3C chemokine receptor 1 (CX3CR1), are known to play a key role in pain and inflammation signaling pathways. Recent studies have shown that the regulation of CX3CR1/L1 signaling influences the development of various diseases including neuronal diseases. We determined whether CX3CR1/L1 signaling is a putative therapeutic target for POCD in a mouse model.

methodsAdult (9-11 weeks) male mice were treated with neutralizing antibody to block CX3CR1/L1 signaling both before and after surgery. Inflammatory and behavioral responses including pain were assessed postoperatively. Also, CX3CR1 mRNA level was assessed. Hippocampal astrocyte activation, Mao B expression, and GABA expression were assessed at 2 days after surgery following neutralizing antibody administration.

resultsThe behavioral response indicated cognitive dysfunction and development of pain in the surgery group compared with the control group. Also, increased levels of pro-inflammatory cytokines and CX3CR1 mRNA were observed in the surgery group. In addition, increased levels of GABA and increased Mao B expression were observed in reactive astrocytes in the surgery group; these responses were attenuated by neutralizing antibody administration.

conclusionsIncreased CX3CR1 after surgery is both necessary and sufficient to induce cognitive dysfunction. CX3CR1 could be an important target for therapeutic strategies to prevent the development of POCD.

Indexed as

AnimalsAstrocytesChemokine CX3CL1CX3C Chemokine Receptor 1Disease Models, Animalgamma-Aminobutyric AcidInflammationMaleMiceOrthopedic ProceduresPostoperative Cognitive ComplicationsSignal TransductionChemokine CX3CL1CX3C Chemokine Receptor 1Cx3cl1 protein, mouseCx3cr1 protein, mousegamma-Aminobutyric AcidCX3C chemokine receptor 1GABAHippocampusInflammationPostoperative cognitive dysfunctionPostoperative pain

Identifiers

PMID33858422
PMCPMC8048361
OpenAlexW3155734877

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.