Evidence map›Paper›PMID 35057820›Full record

ArticleJournal of nanobiotechnology2022

Acute exposure to gold nanoparticles aggravates lipopolysaccharide-induced liver injury by amplifying apoptosis via ROS-mediated macrophage-hepatocyte crosstalk.

Yongjun Yang, Shijun Fan, Qian Chen, Yongling Lu, Yuanfeng Zhu, Xiaoli Chen, Lin Xia, Qianying Huang, Jiang Zheng, Xin Liu

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of nanobiotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

21 citing papers in PubMed, 48 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Yongjun YangMedical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, 400038, China.
Shijun FanMedical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, 400038, China.
Qian ChenMedical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, 400038, China.
Yongling LuMedical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, 400038, China.
Yuanfeng ZhuMedical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, 400038, China.
Xiaoli ChenMedical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, 400038, China.
Lin XiaMedical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, 400038, China.
Qianying HuangMedical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, 400038, China.
Jiang ZhengMedical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, 400038, China.
Xin LiuMedical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, 400038, China. liux0704@tmmu.edu.cn.
Southwest Hospital · CN

Funding

National Natural Science Foundation of China 81873955National Natural Science Foundation of China 82172133
6 · The paper itself

Abstract

backgroundGold nanoparticles (AuNPs) are increasingly utilized in industrial and biomedical fields, thereby demanding a more comprehensive knowledge about their safety. Current toxicological studies mainly focus on the unfavorable biological impact governed by the physicochemical properties of AuNPs, yet the consequences of their interplay with other bioactive compounds in biological systems are poorly understood.

resultsIn this study, AuNPs with a size of 10 nm, the most favorable size for interaction with host cells, were given alone or in combination with bacterial lipopolysaccharide (LPS) in mice or cultured hepatic cells. The results demonstrated that co exposure to AuNPs and LPS exacerbated fatal acute liver injury (ALI) in mice, although AuNPs are apparently non-toxic when administered alone. AuNPs do not enhance systemic or hepatic inflammation but synergize with LPS to upregulate hepatic apoptosis by augmenting macrophage-hepatocyte crosstalk. Mechanistically, AuNPs and LPS coordinate to upregulate NADPH oxidase 2 (NOX2)-dependent reactive oxygen species (ROS) generation and activate the intrinsic apoptotic pathway in hepatic macrophages. Extracellular ROS generation from macrophages is then augmented, thereby inducing calcium-dependent ROS generation and promoting apoptosis in hepatocytes. Furthermore, AuNPs and LPS upregulate scavenger receptor A expression in macrophages and thus increase AuNP uptake to mediate further apoptosis induction.

conclusionsThis study reveals a profound impact of AuNPs in aggravating the hepatotoxic effect of LPS by amplifying ROS-dependent crosstalk in hepatic macrophages and hepatocytes.

Indexed as

HepatocytesAnimalsApoptosisCell CommunicationChemical and Drug Induced Liver Injury, ChronicGoldHEK293 CellsHumansLipopolysaccharidesLiverMacrophagesMaleMetal NanoparticlesMiceMice, Inbred C57BLReactive Oxygen SpeciesGoldLipopolysaccharidesReactive Oxygen SpeciesAcute liver injuryApoptosisAuNPsLipopolysaccharideReactive oxygen species

Identifiers

PMID35057820
PMCPMC8772144
OpenAlexW4205794892

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.