In one paragraphArticle in Hepatology communications, 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
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
17 authors.
Jiaming ChangGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0000-0003-2326-0449 Sizhe LiuGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0009-0000-5528-5574 Xiaobin WuGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0000-0002-1341-411 Qiying XuGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Mengyue LiGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0009-0001-9092-5626 Zhipeng GuoGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0009-0001-8364-413 Hui ChenGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0009-0008-4029-9656 Hezhen WangGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0000-0001-9453-7834 Lili XuDepartment of Clinical Laboratory, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, China.
Jingru YanGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Ming FuGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0000-0003-1400-0258 Boyuan TaoDepartment of Gastrointestinal Surgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Huimin XiaGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0000-0002-0103-1672 Ruizhong ZhangGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0000-0002-4954-7192 Juan HeGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0000-0001-8568-5480 Zhe WenGuangdong Provincial Key Laboratory of Research in Structure Birth Defect Disease, Guangzhou Institute of pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID 0000-0002-6262-1242 Funding
No grant is acknowledged in the PubMed record.
6 · The paper itselfAbstract
backgroundClassical CD14+CD16- monocytes are elevated in biliary atresia (BA); however, their specific role in bile duct injury and the underlying regulatory mechanisms remain unclear. This study aimed to define their contribution to BA pathogenesis, focusing on the NF-κB signaling pathway.
methodsLiver tissues and blood samples from patients with BA and controls were analyzed by single-cell RNA sequencing, flow cytometry, and immunofluorescence. A rhesus rotavirus-induced BA mouse model was used for anti-Ly6C monocyte depletion and NF-κB inhibition (dehydroxymethylepoxyquinomicin). Transcriptomic profiling and cytokine analysis revealed key molecular mechanisms.
resultsClassical monocytes were significantly enriched near the damaged bile ducts in patients with BA and positively correlated with liver injury severity. These monocytes exhibited NF-κB hyperactivation, marked by the upregulation of TNF, IL-1β, Cxcl2, and NLRP3 inflammasome components. RNA-seq revealed BA-specific monocyte clusters with enriched NF-κB signatures. The depletion of classical monocytes (anti-Ly6C) in rhesus rotavirus-induced BA mice reduced biliary inflammation, restored bile duct patency, and improved survival. Pharmacological NF-κB inhibition (dehydroxymethylepoxyquinomicin) similarly attenuated inflammation and liver dysfunction and improved survival in rhesus rotavirus-induced BA mice.
conclusionsClassical CD14+CD16- monocytes are spatially enriched and exhibit NF-κB hyperactivation in BA. Targeting these cells or their NF-κB axis represents a promising therapeutic strategy to mitigate disease progression.
Indexed as
Biliary AtresiaLipopolysaccharide ReceptorsMonocytesNF-kappa BAnimalsBenzamidesCyclohexanonesCytokinesDisease Models, AnimalFemaleHumansLiverMaleMiceSignal TransductionBenzamidesCyclohexanonesCytokinesdehydroxymethylepoxyquinomicinLipopolysaccharide ReceptorsNF-kappa Bbile ductbiliary atresiabiliary epithelial cellsNF-κB signaling pathwaytherapeutic effect
Identifiers
PMID41974027
PMCPMC13075901
What OpenQuestion holds
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LicenceCC BY-NC-ND
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