Evidence map›Paper›PMID 21803030›Full record

ReviewChemico-biological interactions2011

Molecular pathogenesis of hepatic fibrosis and current therapeutic approaches.

Elisabetta Mormone, Joseph George, Natalia Nieto

Open access · greenAbstract readReview
In one paragraph

Review in Chemico-biological interactions, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed
13.8field-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

113 citing papers in PubMed, 245 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Aspirin Attenuates Liver Fibrosis via Autophagy Induction.Journal of cellular and molecular medicine · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Distinct Hemostasis and Blood Composition in Spiny MouseInternational journal of molecular sciences · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

53 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

3 authors at 1 institution in 1 country.

Elisabetta MormoneDivision of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, NY 10029, USA.
Joseph George
Natalia Nieto
Icahn School of Medicine at Mount Sinai · US

Funding

Project 2P20AA017067 · NIAAA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FRIEDMAN, SCOTT L. · 2008 to 2012
$2.5M
ASS, NOS2, AND ALCOHOLIC LIVER DISEASER01AA017733 · NIAAA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI NIETO, NATALIA · 2008 to 2012
$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 5P20 AA017067NIAAA NIH HHS P20 AA017067NIAAA NIH HHS R01 AA017733NIDDK NIH HHS 2R56 DK069286NIDDK NIH HHS 5R01 DK069286NIDDK NIH HHS R01 DK069286NIDDK NIH HHS R56 DK069286
6 · The paper itself

Abstract

The pathogenesis of hepatic fibrosis involves significant deposition of fibrilar collagen and other extracellular matrix proteins. It is a rather dynamic process of wound healing in response to a variety of persistent liver injury caused by factors such as ethanol intake, viral infection, drugs, toxins, cholestasis, and metabolic disorders. Liver fibrosis distorts the hepatic architecture, decreases the number of endothelial cell fenestrations and causes portal hypertension. Key events are the activation and transformation of quiescent hepatic stellate cells into myofibroblast-like cells with the subsequent up-regulation of proteins such as α-smooth muscle actin, interstitial collagens, matrix metalloproteinases, tissue inhibitor of metalloproteinases, and proteoglycans. Oxidative stress is a major contributing factor to the onset of liver fibrosis and it is typically associated with a decrease in the antioxidant defense. Currently, there is no effective therapy for advanced liver fibrosis. In its early stages, liver fibrosis is reversible upon cessation of the causative agent. In this review, we discuss some aspects on the etiology of liver fibrosis, the cells involved, the molecular pathogenesis, and the current therapeutic approaches.

Indexed as

Genetic TherapyHepatic Stellate CellsHepatitis, AlcoholicHepatitis, Viral, HumanHumansLiver CirrhosisMatrix MetalloproteinasesMicroRNAsOxidative StressRNA InterferenceMatrix MetalloproteinasesMicroRNAs

Identifiers

PMID21803030
PMCPMC3171510
OpenAlexW2065348863

What OpenQuestion holds

Textmetadata
LicenceTDM
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.