Evidence map›Paper›PMID 33333846›Full record

ReviewAntioxidants (Basel, Switzerland)2020

Molecular Mechanisms That Link Oxidative Stress, Inflammation, and Fibrosis in the Liver.

Erika Ramos-Tovar, Pablo Muriel

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed, 1 pooled it
22.0field-weighted citation impact, top 1% 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

170 citing papers in PubMed, 1 synthesis or guideline pooled it, 299 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
  6. Article
  7. A copper-deficient diet increases the development of hepatic steatosis, oxidative stress, and mitochondrial dysfunction in mice fed a high-fat diet.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026
    Review
  14. Article
  15. Evaluating the Hepatoprotective Effect ofFood science & nutrition · 2026
    Article
  16. Article
  17. The Liver-Testis Axis: Molecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2026
    Review
  18. Article
  19. Review
  20. Review

110 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.

Erika Ramos-TovarPostgraduate Studies and Research Section, School of Higher Education in Medicine-IPN, Plan de San Luis y Díaz Mirón s/n, Casco de Santo Tomás, Mexico City 11340, Mexico.ORCID 0000-0002-6616-9760
Pablo MurielLaboratory of Experimental Hepatology, Department of Pharmacology, Cinvestav-IPN, Av. Instituto Politécnico Nacional 2508, Apartado Postal 14-740, Mexico City 07000, Mexico.ORCID 0000-0002-2236-6631
Instituto Politécnico Nacional · MX

Funding

Consejo Nacional de Ciencia y Tecnología 53358
6 · The paper itself

Abstract

Activated hepatic stellate cells (HSCs) and myofibroblasts are the main producers of extracellular matrix (ECM) proteins that form the fibrotic tissue that leads to hepatic fibrosis. Reactive oxygen species (ROS) can directly activate HSCs or induce inflammation or programmed cell death, especially pyroptosis, in hepatocytes, which in turn activates HSCs and fibroblasts to produce ECM proteins. Therefore, antioxidants and the nuclear factor E2-related factor-2 signaling pathway play critical roles in modulating the profibrogenic response. The master proinflammatory factors nuclear factor-κB (NF-κB) and the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome may coordinate to produce and activate profibrogenic molecules such as interleukins 1β and 18, which effectively activate HSCs, to produce large amounts of fibrotic proteins. Furthermore, the NLRP3 inflammasome activates pro-caspase 1, which is upregulated by NF-κB, to produce caspase 1, which induces pyroptosis via gasdermin and the activation of HSCs. ROS play central roles in the activation of the NF-κB and NLRP3 signaling pathways via IκB (an inhibitor of NF-κB) and thioredoxin-interacting protein, respectively, thereby linking the molecular mechanisms of oxidative stress, inflammation and fibrosis. Elucidating these molecular pathways may pave the way for the development of therapeutic tools to interfere with specific targets.

Indexed as

extracellular matrixhepatic stellate cellsinflammationliver damageNF-κBNLRP3 inflammasomeNRF2-KEAP1ROS

Identifiers

PMID33333846
PMCPMC7765317
OpenAlexW3111668102

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.