Evidence map›Paper›PMID 26204504›Full record

ReviewRedox biology2015

Role of NADPH oxidases in the redox biology of liver fibrosis.

Eva Crosas-Molist, Isabel Fabregat

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

91 citing papers in PubMed, 143 citations in OpenAlex.

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  20. Emerging role of lipophagy in liver disorders.Molecular and cellular biochemistry · 2024
    Review

31 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 2 institutions in 1 country.

Eva Crosas-MolistBellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet, Barcelona, Spain.
Isabel FabregatBellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet, Barcelona, Spain; Department of Physiological Sciences II, University of Barcelona, L'Hospitalet, Barcelona, Spain. Electronic address: ifabregat@idibell.cat.
Institut d'Investigació Biomédica de Bellvitge · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis is the pathological consequence of chronic liver diseases, where an excessive deposition of extracellular matrix (ECM) proteins occurs, concomitantly with the processes of repair and regeneration. It is characterized by increased production of matrix proteins, in particular collagens, and decreased matrix remodelling. The principal source of ECM accumulation is myofibroblasts (MFB). Most fibrogenic MFB are endogenous to the liver, coming from hepatic stellate cells (HSC) and portal fibroblasts. Dysregulated inflammatory responses have been associated with most (if not all) hepatotoxic insults and chronic oxidative stress play a role during the initial liver inflammatory phase and its progression to fibrosis. Redox-regulated processes are responsible for activation of HSC to MFB, as well as maintenance of the MFB function. Increased oxidative stress also induces hepatocyte apoptosis, which contributes to increase the liver injury and to transdifferentiate HSC to MFB, favouring the fibrogenic process. Mitochondria and other redox-active enzymes can generate superoxide and hydrogen peroxide as a by-product in liver cells. Moreover, accumulating evidence indicates that NADPH oxidases (NOXs), which play a critical role in the inflammatory response, may contribute to reactive oxygen species (ROS) production during liver fibrosis, being important players in HSC activation and hepatocyte apoptosis. Based on the knowledge of the pathogenic role of ROS, different strategies to prevent or reverse the oxidative damage have been developed to be used as therapeutic tools in liver fibrosis. This review will update all these concepts, highlighting the relevance of redox biology in chronic fibrogenic liver pathologies.

Indexed as

AnimalsAntioxidantsAntiviral AgentsEnzyme InhibitorsExtracellular Matrix ProteinsHepatic Stellate CellsHepatocytesHumansLiver CirrhosisMembrane Transport ModulatorsMiceMyofibroblastsNADPH OxidasesOxidation-ReductionOxidative StressReactive Oxygen SpeciesAntioxidantsAntiviral AgentsEnzyme InhibitorsExtracellular Matrix ProteinsMembrane Transport ModulatorsNADPH OxidasesReactive Oxygen SpeciesHepatocyteInflammationMyofibroblastNOXStellate cellTGF-beta

Identifiers

PMID26204504
PMCPMC4804101
OpenAlexW879038605

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.