Evidence map›Paper›PMID 34168124›Full record

ArticleCell death & disease2021

Conditional depletion of macrophages ameliorates cholestatic liver injury and fibrosis via lncRNA-H19.

Xinbei Tian, Ying Wang, Ying Lu, Weipeng Wang, Jun Du, Shanshan Chen, Huiping Zhou, Wei Cai, Yongtao Xiao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
9.0field-weighted citation impact, top 1% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

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  17. Liver Macrophage Diversity in Health and Disease.Results and problems in cell differentiation · 2024
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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 at 5 institutions in 2 countries.

Xinbei Tian *Division of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Ying Wang *Division of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Ying LuShanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai, China.
Weipeng WangDepartment of Pediatric Surgery, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Jun DuShanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai, China.
Shanshan ChenDivision of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Huiping ZhouDepartment of Microbiology and Immunology and McGuire Veterans AfSfairs Medical Center, Virginia Commonwealth University, Richmond, VA, USA.ORCID 0000-0002-0050-372X
Wei CaiDivision of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. caiw204@sjtu.edu.cn.
Yongtao XiaoDivision of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. xiaoyongtao@xinhuamed.com.cn.ORCID 0000-0002-0964-609X
Shanghai Jiao Tong University · CNShanghai Institute of Nutrition and Health · CNShanghai University · CNVirginia Commonwealth University · USXinHua Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81770517
6 · The paper itself

Abstract

Although macrophages are recognized as important players in the pathogenesis of chronic liver diseases, their roles in cholestatic liver fibrosis remain incompletely understood. We previously reported that long noncoding RNA-H19 (lncRNA-H19) contributes to cholangiocyte proliferation and cholestatic liver fibrosis of biliary atresia (BA). We here show that monocyte/macrophage CD11B mRNA levels are increased significantly in livers of BA patients and positively correlated with the progression of liver inflammation and fibrosis. The macrophages increasingly infiltrate and accumulate in the fibrotic niche and peribiliary areas in livers of BA patients. Selective depletion of macrophages using the transgenic CD11b-diphtheria toxin receptor (CD11b-DTR) mice halts bile duct ligation (BDL)-induced progression of liver damage and fibrosis. Meanwhile, macrophage depletion significantly reduces the BDL-induced hepatic lncRNA-H19. Overexpression of H19 in livers using adeno-associated virus serotype 9 (AAV9) counteracts the effects of macrophage depletion on liver fibrosis and cholangiocyte proliferation. Additionally, both H19 knockout (H19

Indexed as

Macrophage ActivationAnimalsCase-Control StudiesCD11b Antigencdc42 GTP-Binding ProteinCell ProliferationCholestasisHeparin-binding EGF-like Growth FactorHumansLiverLiver Cirrhosis, BiliaryLiver Cirrhosis, ExperimentalMacrophagesMiceMice, Inbred C57BLMice, KnockoutCD11b Antigencdc42 GTP-Binding ProteinCDC42 protein, humanH19 long non-coding RNAHeparin-binding EGF-like Growth FactorItgam protein, mouserhoA GTP-Binding ProteinRNA, Long Noncoding

Identifiers

PMID34168124
PMCPMC8225916
OpenAlexW3173529774

What OpenQuestion holds

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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.