Evidence map›Paper›PMID 28874845›Full record

ArticleScientific reports2017

M2-like macrophages in the fibrotic liver protect mice against lethal insults through conferring apoptosis resistance to hepatocytes.

Li Bai, Xin Liu, Qingfen Zheng, Ming Kong, Xiaohui Zhang, Richard Hu, Jinli Lou, Feng Ren, Yu Chen, Sujun Zheng and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 53 citations in OpenAlex.

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  15. [Liver fibrosis inhibits lethal injury through D-galactosamine/lipopolysaccharide-induced necroptosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022
    Article
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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

14 authors at 5 institutions in 2 countries.

Li BaiArtificial Liver Center, Beijing YouAn Hospital, Capital Medical University, Beijing, 100069, China.
Xin LiuArtificial Liver Center, Beijing YouAn Hospital, Capital Medical University, Beijing, 100069, China.
Qingfen ZhengArtificial Liver Center, Beijing YouAn Hospital, Capital Medical University, Beijing, 100069, China.
Ming KongArtificial Liver Center, Beijing YouAn Hospital, Capital Medical University, Beijing, 100069, China.
Xiaohui ZhangArtificial Liver Center, Beijing YouAn Hospital, Capital Medical University, Beijing, 100069, China.
Richard HuOlive View-UCLA Medical Center, Los Angeles, CA, 91342, USA.
Jinli LouArtificial Liver Center, Beijing YouAn Hospital, Capital Medical University, Beijing, 100069, China.
Feng RenBeijing Institute of Liver Diseases, Beijing, 100069, China.
Yu ChenArtificial Liver Center, Beijing YouAn Hospital, Capital Medical University, Beijing, 100069, China.
Sujun ZhengArtificial Liver Center, Beijing YouAn Hospital, Capital Medical University, Beijing, 100069, China.
Shuang LiuArtificial Liver Center, Beijing YouAn Hospital, Capital Medical University, Beijing, 100069, China.
Yuan-Ping HanThe Center for Growth, Metabolism and Aging, the Key Laboratory for Bio-Resource and Eco-Environment, College of Life Sciences, and the National Key Laboratory of Biotherapy, Sichuan University, Chengdu, 610014, China. hanyp@scu.edu.cn.
Zhongping DuanArtificial Liver Center, Beijing YouAn Hospital, Capital Medical University, Beijing, 100069, China. duan2517@163.com.
Stephen J PandolCedars-Sinai Medical Center, and Department of Veterans Affairs, Los Angeles, CA90048, USA.
Beijing YouAn Hospital · CNCapital Medical University · CNCedars-Sinai Medical Center · USOlive View-UCLA Medical Center · USSichuan University · CN

Funding

The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANNA S. GUKOVSKAYA · 1999 to 2026
$45.8M
Targeting diet-induced promotion of Kras-initiated pancreatic adenocarcinomaP01CA163200 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PANDOL, STEPHEN J. · 2012 to 2016
$6.2M
NCI NIH HHS P01 CA163200NIAAA NIH HHS P50 AA011999
6 · The paper itself

Abstract

Acute injury in the setting of liver fibrosis is an interesting and still unsettled issue. Most recently, several prominent studies have indicated the favourable effects of liver fibrosis against acute insults. Nevertheless, the underlying mechanisms governing this hepatoprotection remain obscure. In the present study, we hypothesized that macrophages and their M1/M2 activation critically involve in the hepatoprotection conferred by liver fibrosis. Our findings demonstrated that liver fibrosis manifested a beneficial role for host survival and apoptosis resistance. Hepatoprotection in the fibrotic liver was tightly related to innate immune tolerance. Macrophages undertook crucial but divergent roles in homeostasis and fibrosis: depleting macrophages in control mice protected from acute insult; conversely, depleting macrophages in fibrotic liver weakened the hepatoprotection and gave rise to exacerbated liver injury upon insult. The contradictory effects of macrophages can be ascribed, to a great extent, to the heterogeneity in macrophage activation. Macrophages in fibrotic mice exhibited M2-preponderant activation, which was not the case in acutely injured liver. Adoptive transfer of M2-like macrophages conferred control mice conspicuous protection against insult. In vitro, M2-polarized macrophages protected hepatocytes against apoptosis. Together, M2-like macrophages in fibrotic liver exert the protective effects against lethal insults through conferring apoptosis resistance to hepatocytes.

Indexed as

ApoptosisAdoptive TransferAnimalsCells, CulturedHepatocytesImmune ToleranceImmunity, InnateLiver CirrhosisMacrophage ActivationMacrophagesMaleMiceMice, Inbred BALB C

Identifiers

PMID28874845
PMCPMC5585332
OpenAlexW2750908099

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.