Evidence map›Paper›PMID 17531188›Full record

ReviewArchives of biochemistry and biophysics2007

NOX in liver fibrosis.

Samuele De Minicis, David A Brenner

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Archives of biochemistry and biophysics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01598064 (Clinical Trial of Probiotics in Preventing Complication Related to Portal Hypertension in Cirrhotic Patients), which is not on this map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
7.4field-weighted citation impact, top 2% 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.

NCT01598064 nacompletednot on this mapstarted 2012, after this paper: background citation

Clinical Trial of Probiotics in Preventing Complication Related to Portal Hypertension in Cirrhotic Patients

TypeinterventionalSponsorPo-Lin Chen, MDRan2012 to 2013Enrolled49ConditionsLiver Cirrhosis, Portal HypertensionArmsGK#10, Placebo
3 · Its place in the literature

Who cites it

69 citing papers in PubMed, 159 citations in OpenAlex.

  1. Trial
  2. Pathogenesis, Non-Invasive Assessments and Treatment of Hepatic Fibrosis in Autoimmune Liver Diseases.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Cellular heterogeneity and plasticity during NAFLD progression.Frontiers in molecular biosciences · 2023
    Review
  7. Review
  8. Article
  9. Review
  10. The Overactivation of NADPH Oxidase duringAntioxidants (Basel, Switzerland) · 2021
    Article
  11. Article
  12. Liver Fibrosis: Therapeutic Targets and Advances in Drug Therapy.Frontiers in cell and developmental biology · 2021
    Review
  13. Article
  14. Review
  15. Mechanisms of liver fibrosis and its role in liver cancer.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  16. Article
  17. Apocynin Dietary Supplementation Delays Mouse Ovarian Ageing.Oxidative medicine and cellular longevity · 2019
    Article
  18. Review
  19. Hepatic Fibrosis in Dogs.Journal of veterinary internal medicine · 2018
    Review
  20. Article

9 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

2 authors at 1 institution in 1 country.

Samuele De MinicisDepartment of Medicine, Columbia University, College of Physicians and Surgeons, New York, NY 10026, USA.
David A Brenner
Columbia University · US

Funding

Angiotensin II and NADPH Oxidase in Hepatic FibrosisR01DK072237 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BRENNER, DAVID A. · 2005 to 2009
$1.7M
NIDDK NIH HHS R01 DK072237
6 · The paper itself

Abstract

NADPH oxidase is a multi-protein complex producing reactive oxygen species (ROS) both in phagocytic cells, being essential in host defense, and in non-phagocytic cells, regulating intracellular signalling. In the liver, NADPH oxidase plays a central role in fibrogenesis. A functionally active form of the NADPH oxidase is expressed not only in Kupffer cells (phagocytic cell type) but also in hepatic stellate cells (HSCs) (non-phagocytic cell type), suggesting a role of the non-phagocytic NADPH oxidase in HSC activation. Consistent with this concept, profibrogenic agonists such as Angiotensin II (Ang II) and platelet derived growth factor (PDGF), or apoptotic bodies exert their activity through NADPH oxidase-activation in HSCs. Both pharmacological inhibition with DPI and genetic studies using p47(phox) knockout mice provided evidence for a central role of NADPH oxidase in the regulation of HSC-activity and liver fibrosis. In addition to the p47(phox) component, only Rac1 has been identified as a functional active component of the NADPH oxidase complex in HSCs.

Indexed as

ApoptosisModels, BiologicalAnimalsApoptosis Regulatory ProteinsHumansLiverLiver CirrhosisNADPH OxidasesOxidative StressReactive Oxygen SpeciesSignal TransductionApoptosis Regulatory ProteinsNADPH OxidasesReactive Oxygen Species

Identifiers

PMID17531188
PMCPMC2727549
OpenAlexW2001855707

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.