Evidence map›Paper›PMID 21371444›Full record

ArticleBiochemical pharmacology2011

EGCG stimulates autophagy and reduces cytoplasmic HMGB1 levels in endotoxin-stimulated macrophages.

Wei Li, Shu Zhu, Jianhua Li, Andrei Assa, Arvin Jundoria, Jianying Xu, Saijun Fan, N Tony Eissa, Kevin J Tracey, Andrew E Sama and 1 more

Open access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 1 pooled it
9.8field-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

99 citing papers in PubMed, 1 synthesis or guideline pooled it, 168 citations in OpenAlex.

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39 more citing papers are in PubMed but not listed here.

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

11 authors at 4 institutions in 2 countries.

Wei LiThe Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030, USA.
Shu Zhu
Jianhua Li
Andrei Assa
Arvin Jundoria
Jianying Xu
Saijun Fan
N Tony Eissa
Kevin J Tracey
Andrew E Sama
Haichao Wang
Feinstein Institute for Medical Research · USSoochow University · CNBaylor College of Medicine · USNorth Shore University Hospital · US

Funding

Mechanisms of Novel Herbal Therapies for Sepsis.R01AT005076 · NCCIH · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI WANG, HAICHAO · 2010 to 2023
$4.3M
Regulation of HMGB1 Release in Endotoxemia.R01GM063075 · NIGMS · NORTH SHORE UNIVERSITY HOSPITAL · PI WANG, HAICHAO · 2002 to 2020
$4.2M
HMG IN POST OPERATIVE AND TRAUMATIC STRESSR01GM062508 · NIGMS · NORTH SHORE UNIVERSITY HOSPITAL · PI TRACEY, KEVIN J · 2001 to 2014
$3.7M
NCCIH NIH HHS R01 AT005076NCCIH NIH HHS R01AT005076NIGMS NIH HHS R01 GM062508NIGMS NIH HHS R01 GM063075NIGMS NIH HHS R01GM063075
6 · The paper itself

Abstract

Historically, consumption of Green tea (Camellia sinensis) has been associated with health benefits against multiple diseases including cancer, atherosclerosis and cardiovascular disorders. Emerging evidence has suggested a pathogenic role for HMGB1, a newly identified "late" mediator of lethal systemic inflammation, in the aforementioned diseases. Here we demonstrated that a major ingredient of Green tea, EGCG, was internalized into HMGB1-containing LC3-positive cytoplasmic vesicles (likely autophagosomes) in macrophages, and induced HMGB1 aggregation in a time-dependent manner. Furthermore, EGCG stimulated LC3-II production and autophagosome formation, and inhibited LPS-induced HMGB1 up-regulation and extracellular release. The EGCG-mediated HMGB1 inhibitory effects were diminished by inhibition of class III phosphatidylinositol-3 kinase (with 3-methyladenine) or knockdown of an essential autophagy-regulating protein, beclin-1. Moreover, the EGCG-mediated protection against lethal sepsis was partly impaired by co-administration of an autophagy inhibitor, chloroquine. Taken together, the present study has suggested a possibility that EGCG inhibits HMGB1 release by stimulating its autophagic degradation.

Indexed as

AnimalsAutophagyBlotting, WesternCatechinCell LineCytoplasmHMGB1 ProteinLipopolysaccharidesMacrophagesMaleMiceMice, Inbred BALB CMicroscopy, Electron, TransmissionRatsRNA InterferenceCatechinepigallocatechin gallateHMGB1 ProteinLipopolysaccharides

Identifiers

PMID21371444
PMCPMC3072446
OpenAlexW1982348992

What OpenQuestion holds

Textmetadata
LicenceTDM
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.