Evidence map›Paper›PMID 36290761›Full record

ReviewAntioxidants (Basel, Switzerland)2022

NOX as a Therapeutic Target in Liver Disease.

Deyamira Matuz-Mares, Héctor Vázquez-Meza, María Magdalena Vilchis-Landeros

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
7.2field-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.

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

33 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  4. New therapies for primary biliary cholangitis.Hepatology international · 2026
    Review
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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

3 authors at 1 institution in 1 country.

Deyamira Matuz-MaresDepartamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Coyoacán, Ciudad de México CP 04510, Mexico.
Héctor Vázquez-MezaDepartamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Coyoacán, Ciudad de México CP 04510, Mexico.ORCID 0000-0002-8312-3115
María Magdalena Vilchis-LanderosDepartamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Coyoacán, Ciudad de México CP 04510, Mexico.
Universidad Nacional Autónoma de México · MX

Funding

National Autonomous University of Mexico IN-218821National Autonomous University of Mexico PP012Matuz
6 · The paper itself

Abstract

The nicotinamide adenine dinucleotide phosphate hydrogen oxidase (NADPH oxidase or NOX) plays a critical role in the inflammatory response and fibrosis in several organs such as the lungs, pancreas, kidney, liver, and heart. In the liver, NOXs contribute, through the generation of reactive oxygen species (ROS), to hepatic fibrosis by acting through multiple pathways, including hepatic stellate cell activation, proliferation, survival, and migration of hepatic stellate cells; hepatocyte apoptosis, enhancement of fibrogenic mediators, and mediation of an inflammatory cascade in both Kupffer cells and hepatic stellate cells. ROS are overwhelmingly produced during malignant transformation and hepatic carcinogenesis (HCC), creating an oxidative microenvironment that can cause different and various types of cellular stress, including DNA damage, ER stress, cell death of damaged hepatocytes, and oxidative stress. NOX1, NOX2, and NOX4, members of the NADPH oxidase family, have been linked to the production of ROS in the liver. This review will analyze some diseases related to an increase in oxidative stress and its relationship with the NOX family, as well as discuss some therapies proposed to slow down or control the disease's progression.

Indexed as

cancerfibrosisliverNOXROS

Identifiers

PMID36290761
PMCPMC9598239
OpenAlexW4306362488

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.