Evidence map›Paper›PMID 24219114›Full record

ReviewAntioxidants & redox signaling2014

Extracellular matrix and liver disease.

Elena Arriazu, Marina Ruiz de Galarreta, Francisco Javier Cubero, Marta Varela-Rey, María Pilar Pérez de Obanos, Tung Ming Leung, Aritz Lopategi, Aitor Benedicto, Ioana Abraham-Enachescu, Natalia Nieto

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

96 citing papers in PubMed, 185 citations in OpenAlex.

  1. Trial
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  9. A One-Dimensional (1D) Computational Fluid Dynamics Study of Fontan-Associated Liver Disease (FALD).International journal for numerical methods in biomedical engineering · 2026
    Article
  10. Review
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36 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

10 authors at 7 institutions in 5 countries.

Elena Arriazu1 Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine , New York, New York.
Marina Ruiz de Galarreta
Francisco Javier Cubero
Marta Varela-Rey
María Pilar Pérez de Obanos
Tung Ming Leung
Aritz Lopategi
Aitor Benedicto
Ioana Abraham-Enachescu
Natalia Nieto
Icahn School of Medicine at Mount Sinai · USCIC bioGUNE · ESEtna Biotech (Italy) · ITRWTH Aachen University · DESUNY Downstate Health Sciences University · USToshiba (Japan) · JPUniversidad Publica de Navarra · ES

Funding

Project 2P20AA017067 · NIAAA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FRIEDMAN, SCOTT L. · 2008 to 2012
$2.5M
Milk osteopontin, a nutritional therapeutic intervention for alcoholic hepatitisU01AA021887 · NIAAA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NIETO, NATALIA · 2012 to 2017
$2.0M
Communication between Kupffer cells and stellate cellsR01DK069286 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI NIETO, NATALIA · 2005 to 2009
$1.2M
Osteopontin and the fibrogenic response to liver injuryR56DK069286 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI NIETO, NATALIA · 2010 to 2012
$544k
NIAAA NIH HHS 5 P20 AA017067NIAAA NIH HHS 5 P20 AA017067-01S1NIAAA NIH HHS 5 P20 AA017067-03S1NIAAA NIH HHS U01 AA021887-01NIDDK NIH HHS 2R56 DK069286NIDDK NIH HHS 3 R56 DK069286-06S1NIDDK NIH HHS 5R01 DK069286
6 · The paper itself

Abstract

significanceThe extracellular matrix (ECM) is a dynamic microenvironment that undergoes continuous remodeling, particularly during injury and wound healing. Chronic liver injury of many different etiologies such as viral hepatitis, alcohol abuse, drug-induced liver injury, obesity and insulin resistance, metabolic disorders, and autoimmune disease is characterized by excessive deposition of ECM proteins in response to persistent liver damage. CRITICAL ISSUES: This review describes the main collagenous and noncollagenous components from the ECM that play a significant role in pathological matrix deposition during liver disease. We define how increased myofibroblasts (MF) from different origins are at the forefront of liver fibrosis and how liver cell-specific regulation of the complex scarring process occurs. RECENT ADVANCES: Particular attention is paid to the role of cytokines, growth factors, reactive oxygen species, and newly identified matricellular proteins in the regulation of fibrillar type I collagen, a field to which our laboratory has significantly contributed over the years. We compile data from recent literature on the potential mechanisms driving fibrosis resolution such as MF' apoptosis, senescence, and reversal to quiescence. FUTURE DIRECTIONS: We conclude with a brief description of how epigenetics, an evolving field, can regulate the behavior of MF and of how new "omics" tools may advance our understanding of the mechanisms by which the fibrogenic response to liver injury occurs.

Indexed as

AnimalsApoptosisExtracellular MatrixHumansLiverLiver DiseasesMyofibroblasts

Identifiers

PMID24219114
PMCPMC4123471
OpenAlexW2050739087

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.