Evidence map›Paper›PMID 24492281›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2014

Modulation of PI3K-LXRα-dependent lipogenesis mediated by oxidative/nitrosative stress contributes to inhibition of HCV replication by quercetin.

Sandra Pisonero-Vaquero, María V García-Mediavilla, Francisco Jorquera, Pedro L Majano, Marta Benet, Ramiro Jover, Javier González-Gallego, Sonia Sánchez-Campos

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In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Frontiers in microbiology · 2024
    Review
  5. Article
  6. Targeting BRD4 and PI3K signaling pathways for the treatment of medulloblastoma.Journal of controlled release : official journal of the Controlled Release Society · 2023
    Article
  7. Focus on the high therapeutic potentials of quercetin and its derivatives.Phytomedicine plus : international journal of phytotherapy and phytopharmacology · 2022
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Apigenin Attenuates Adriamycin-Induced Cardiomyocyte Apoptosis via the PI3K/AKT/mTOR Pathway.Evidence-based complementary and alternative medicine : eCAM · 2017
    Article
  19. Article
  20. Article
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

8 authors at 6 institutions in 1 country.

Sandra Pisonero-VaqueroInstitute of Biomedicine (IBIOMED), University of León, León, Spain.
María V García-Mediavilla1] Institute of Biomedicine (IBIOMED), University of León, León, Spain [2] Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain.
Francisco Jorquera1] Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain [2] Department of Gastroenterology, Complejo Asistencial Universitario de León, León, Spain.
Pedro L Majano1] Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain [2] Molecular Biology Unit, Hospital Universitario de la Princesa, Instituto de Investigación Sanitaria Princesa (IP), Madrid, Spain.
Marta Benet1] Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain [2] Experimental Hepatology Unit, IIS Hospital La Fe, Valencia, Spain.
Ramiro Jover1] Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain [2] Experimental Hepatology Unit, IIS Hospital La Fe, Valencia, Spain [3] Department of Biochemistry and Molecular Biology, University of Valencia, Valencia, Spain.
Javier González-Gallego1] Institute of Biomedicine (IBIOMED), University of León, León, Spain [2] Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain.
Sonia Sánchez-Campos1] Institute of Biomedicine (IBIOMED), University of León, León, Spain [2] Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain.
Universidad de León · ESCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESComplejo Asistencial Universitario de Palencia · ESHospital Universitario de La Princesa · ESInstituto de Investigación Sanitaria La Fe · ESInstituto de Salud Carlos III · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is experimental evidence that some antioxidant flavonoids show therapeutic potential in the treatment of hepatitis C through inhibition of hepatitis C virus (HCV) replication. We examined the effect of treatment with the flavonols quercetin and kaempferol, the flavanone taxifolin and the flavone apigenin on HCV replication efficiency in an in vitro model. While all flavonoids studied were able to reduce viral replication at very low concentrations (ranging from 0.1 to 5 μM), quercetin appeared to be the most effective inhibitor of HCV replication, showing a marked anti-HCV activity in replicon-containing cells when combined with interferon (IFN)α. The contribution of oxidative/nitrosative stress and lipogenesis modulation to inhibition of HCV replication by quercetin was also examined. As expected, quercetin decreased HCV-induced reactive oxygen and nitrogen species (ROS/RNS) generation and lipoperoxidation in replicating cells. Quercetin also inhibited liver X receptor (LXR)α-induced lipid accumulation in LXRα-overexpressing and replicon-containing Huh7 cells. The mechanism underlying the LXRα-dependent lipogenesis modulatory effect of quercetin in HCV-replicating cells seems to involve phosphatidylinositol 3-kinase (PI3K)/AKT pathway inactivation. Thus, inhibition of the PI3K pathway by LY294002 attenuated LXRα upregulation and HCV replication mediated by lipid accumulation, showing an additive effect when combined with quercetin. Inactivation of the PI3K pathway by quercetin may contribute to the repression of LXRα-dependent lipogenesis and to the inhibition of viral replication induced by the flavonol. Combined, our data suggest that oxidative/nitrosative stress blockage and subsequent modulation of PI3K-LXRα-mediated lipogenesis might contribute to the inhibitory effect of quercetin on HCV replication.

Indexed as

AntioxidantsAntiviral AgentsApigeninCell LineChromonesDown-RegulationFatty Acids, NonesterifiedHepacivirusHumansKaempferolsLipogenesisLiver X ReceptorsMorpholinesOrphan Nuclear ReceptorsOxidative StressPhosphatidylinositol 3-Kinases2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAntioxidantsAntiviral AgentsApigeninChromonesFatty Acids, NonesterifiedkaempferolKaempferolsLiver X ReceptorsMorpholinesNR1H3 protein, humanOrphan Nuclear ReceptorsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktQuercetinReactive Nitrogen SpeciestaxifolinTriglycerides

Identifiers

PMID24492281
OpenAlexW2056620630

What OpenQuestion holds

Textmetadata
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.