Evidence map›Paper›PMID 39261768›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

SYK promotes the formation of neutrophil extracellular traps by inducing PKM2 nuclear translocation and promoting STAT3 phosphorylation to exacerbate hepatic ischemia-reperfusion injury and tumor recurrence.

Xuejiao Chen, Chuanwei Jiang, Minhao Chen, Xiangdong Li, Wenjie Yu, Aigang Qiu, Linfeng Sun, Liyong Pu, Yuhua Shi

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Review
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  4. PKM2: A gatekeeper in macrophage metabolic reprogramming.Journal of pharmaceutical analysis · 2026
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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.

Xuejiao Chen *Department of General Surgery, The Yancheng School of Clinical Medicine of Nanjing Medical University, 75 Theater Road, Yancheng, 224000, Jiangsu province, China.
Chuanwei Jiang *Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210003, Jiang Su province, China.
Minhao Chen *Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210003, Jiang Su province, China.
Xiangdong LiHepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210003, Jiang Su province, China.
Wenjie YuHepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210003, Jiang Su province, China.
Aigang QiuDepartment of General Surgery, The Yancheng School of Clinical Medicine of Nanjing Medical University, 75 Theater Road, Yancheng, 224000, Jiangsu province, China.
Linfeng SunHepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210003, Jiang Su province, China.
Liyong PuHepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210003, Jiang Su province, China. puliyong@njmu.edu.cn.
Yuhua ShiDepartment of General Surgery, The Yancheng School of Clinical Medicine of Nanjing Medical University, 75 Theater Road, Yancheng, 224000, Jiangsu province, China. ycsypwk@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAt present, hepatic ischemia-reperfusion injury (IRI) is an important complication of partial hepatectomy and liver transplantation, and it is an important cause of poor prognosis. Spleen tyrosine kinase(SYK) plays an important role in a variety of signaling pathways in the liver, but its role in hepatic IRI is still unclear. This study aims to investigate the role and mechanism of SYK in hepatic IRI and tumor recurrence.

methodsWe first observed the activation of SYK in the liver of mice in response to hepatic IRI. Subsequently, Pharmacological inhibitions of SYK were used to evaluated the effect of SYK on neutrophil recruitment and NETosis, and further explored the effect of SYK on IRI and tumor recurrence.

resultsOur study shows that SYK is activated in response to hepatic IRI and aggravates liver injury. On the one hand, neutrophils SYK during the early stage of liver reperfusion increases neutrophil extracellular traps (NETs) production by promoting Pyruvate kinase M2(PKM2) nuclear translocation leading to upregulation of phosphorylated STAT3, thereby exacerbating liver inflammation and tumor recurrence. On the other hand, macrophages SYK can promote the recruitment of neutrophils and increase the activation of NLRP3 inflammasome and IL1β, which further promotes the formation of NETs.

conclusionsOur study demonstrates that neutrophil and macrophage SYK synergistically promote hepatic IRI and tumor recurrence, and SYK may be a potential target to improve postoperative hepatic IRI and tumor recurrence.

Indexed as

Extracellular TrapsMembrane ProteinsNeutrophilsReperfusion InjurySTAT3 Transcription FactorSyk KinaseAnimalsCarrier ProteinsDisease Models, AnimalHumansLiverLiver NeoplasmsMaleMiceMice, Inbred C57BLNeoplasm Recurrence, LocalCarrier ProteinsMembrane ProteinsPkm protein, mousePyruvate KinaseSTAT3 Transcription FactorSyk KinaseSyk protein, mouseThyroid Hormone-Binding ProteinsIschemia-reperfusion injuryMacrophageNeutrophil Extracellular traps

Identifiers

PMID39261768
PMCPMC11391729

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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.