Evidence map›Paper›PMID 21098019›Full record

ArticleThe Journal of biological chemistry2011

HIV and HCV cooperatively promote hepatic fibrogenesis via induction of reactive oxygen species and NFkappaB.

Wenyu Lin, Guoyang Wu, Shaoyong Li, Ethan M Weinberg, Kattareeya Kumthip, Lee F Peng, Jorge Méndez-Navarro, Wen-Chi Chen, Nikolaus Jilg, Hong Zhao and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 105 citations in OpenAlex.

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  11. Expert Panel Review on Nonalcoholic Fatty Liver Disease in Persons With Human Immunodeficiency Virus.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2022
    Review
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  20. Review

10 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

15 authors at 4 institutions in 3 countries.

Wenyu LinGastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.
Guoyang Wu
Shaoyong Li
Ethan M Weinberg
Kattareeya Kumthip
Lee F Peng
Jorge Méndez-Navarro
Wen-Chi Chen
Nikolaus Jilg
Hong Zhao
Kaku Goto
Leiliang Zhang
Mark A Brockman
Detlef Schuppan
Raymond T Chung
Massachusetts General Hospital · USHarvard University · USBeth Israel Deaconess Medical Center · USSimon Fraser University · CA

Funding

Virology CoreU19AI082630 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG, GEORG Michael LAUER · 2009 to 2026
$48.1M
Viral, T Cell, &Cytokine Determinants of Stellate CellU19AI066313 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SCHUPPAN, DETLEF · 2005 to 2009
$2.6M
HIV-Hepatitis C Virus Interactions and PathogenesisR01AI069939 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI CHUNG, RAYMOND T · 2006 to 2010
$1.9M
Patient-Oriented Research on Hepatitis in Special PopulationsK24DK078772 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI CHUNG, RAYMOND T · 2007 to 2016
$1.6M
NIAID NIH HHS AI066313U19NIAID NIH HHS AI069939NIAID NIH HHS AI082630NIAID NIH HHS R01 AI069939NIAID NIH HHS U19 AI066313NIAID NIH HHS U19 AI082630NIDDK NIH HHS K24 DK078772
6 · The paper itself

Abstract

HIV/HCV coinfection leads to accelerated hepatic fibrosis progression, with higher rates of cirrhosis, liver failure, and liver death than does HCV mono-infection. However, the profibrogenic role of HIV on hepatocytes and hepatic stellate cells (HSC) has not been fully clarified. We hypothesized that HIV, HCV induce liver fibrosis through altered regulation of the production of extracellular matrix and matrix metalloproteinases. We examined the fibrogenesis- and fibrolysis-related gene activity in LX2 HSC and Huh7.5.1 cells in the presence of inactivated CXCR4 and CCR5 HIV, as well as HCV JFH1 virus. The role of reactive oxygen species (ROS) upon fibrosis gene expression was assessed using the ROS inhibitor. Fibrosis-related transcripts including procollagen α1(I) (CoL1A), TIMP1, and MMP3 mRNA were measured by qPCR. TIMP1 and MMP3 protein expression were assessed by ELISA. We found that inactivated CXCR4 HIV and CCR5 HIV increased CoL1A, and TIMP1 expression in both HSC and Huh7.5.1 cells; the addition of JFH1 HCV further increased CoL1A and TIMP1 expression. CXCR4 HIV and CCR5 HIV induced ROS production in HSC and Huh7.5.1 cells which was further enhanced by JFH1 HCV. The ROS inhibitor DPI abrogated HIV-and HCV-induced CoL1A and TIMP1 expression. HIV and HCV-induced CoL1A and TIMP1 expression were also blocked by NFκB siRNA. Our data provide further evidence that HIV and HCV independently regulate hepatic fibrosis progression through the generation of ROS; this regulation occurs in an NFκB-dependent fashion. Strategies to limit the viral induction of oxidative stress are warranted to inhibit fibrogenesis.

Indexed as

Hepatitis CHIV InfectionsLiver CirrhosisCell Line, TumorGene Expression RegulationHepacivirusHIVHumansNF-kappa BOxidative StressReactive Oxygen SpeciesNF-kappa BReactive Oxygen Species

Identifiers

PMID21098019
PMCPMC3024762
OpenAlexW2089532460

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.