Evidence map›Paper›PMID 41649592›Full record

ArticleInflammation2026

Oxidized Phospholipids Aggravate Hepatic Ischemia/Reperfusion Injury by Promoting Macrophage M1 Polarization Via Regulating the Wnt/β-catenin/Autophagy Axis.

Minhao Chen, Yue Liu, Jie Li, Ziyi Wang, Yu Zhang, Xuejiao Chen, Xiangdong Li, Nan Xia, Wenjie Yu, Linfeng Sun and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Minhao Chen *Hepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Yue Liu *Department of General Surgery, Affiliated Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, China.
Jie Li *Hepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Ziyi WangHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Yu ZhangHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Xuejiao ChenHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Xiangdong LiHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Nan XiaHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Wenjie YuHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Linfeng SunHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Yuhao XiaoHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Haoliang ZhuHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Jie WeiHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China.
Liyong PuHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China. puliyong@njmu.edu.cn.
Sheng HanHepatobiliary Center, Key Laboratory of Liver Transplantation, NHC Key Laboratory of Hepatobiliary cancers, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, Nanjing, 210029, Jiangsu Province, China. hansheng@jsph.org.cn.

Funding

National Natural Science Foundation of China 81870443
6 · The paper itself

Abstract

Hepatic ischemia-reperfusion injury (IRI) remains an unavoidable consequence of partial hepatic resection and liver transplantation. Oxidative stress damages cellular lipid membranes, causing the formation of oxidized phospholipids (OxPLs), which are members of damage-associated molecular patterns (DAMPs). Nevertheless, the precise mechanism and significance of OxPLs in hepatic IRI are yet to be investigated. Our findings reveal that OxPLs accumulate excessively in the liver after IR. Compared to the control group, pre-treatment with E06 (an OxPLs-neutralizing antibody) significantly alleviates inflammatory cell infiltration and liver injury following IR. In vitro experiments show that OxPLs inhibit macrophage autophagy, thereby promoting M1 polarization. This regulatory effect depends on the activation of the Wnt/β-Catenin pathway by OxPLs.

Indexed as

AutophagyLiverMacrophagesPhospholipidsReperfusion InjuryWnt Signaling PathwayAnimalsbeta CateninMaleMiceOxidation-ReductionOxidative Stressbeta CateninPhospholipidsAutophagyHepatic ischemia reperfusion injuryMacrophageOxidized phospholipidsWnt/β-catenin

Identifiers

PMID41649592
PMCPMC12920291

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.