Evidence map›Paper›PMID 30766956›Full record

ReviewHepatology communications2019

Combatting Fibrosis: Exosome-Based Therapies in the Regression of Liver Fibrosis.

Li Chen, David A Brenner, Tatiana Kisseleva

Open access · goldAbstract readReview
In one paragraph

Review in Hepatology communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
6.8field-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

56 citing papers in PubMed, 88 citations in OpenAlex.

  1. Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Role of Exosomal Modulation of Macrophages in Liver Fibrosis.Journal of clinical and translational hepatology · 2024
    Review
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.

Li ChenDepartment of Medicine University of California San Diego La Jolla CA.
David A BrennerDepartment of Medicine University of California San Diego La Jolla CA.
Tatiana KisselevaDepartment of Surgery University of California San Diego La Jolla CA.
University of California, San Diego · US

Funding

The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANNA S. GUKOVSKAYA · 1999 to 2026
$45.8M
Inactivation of Hepatic Stellate Cells During Reversal of Liver FibrosisR01DK099205 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BRENNER, DAVID A., KISSELEVA, TATIANA · 2014 to 2025
$4.8M
The Role of Portal Fibroblasts in Cholestatic Liver FibrosisR01DK101737 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KISSELEVA, TATIANA · 2014 to 2025
$3.8M
The role of IL-17 signaling in alcohol-induced HCCR01AA028550 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BRENNER, DAVID A., KISSELEVA, TATIANA · 2021 to 2025
$2.3M
Fibrocytes regulate liver fibrosisR01DK111866 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KISSELEVA, TATIANA · 2017 to 2020
$1.4M
NIAAA NIH HHS P50 AA011999NIAAA NIH HHS R01 AA028550NIDDK NIH HHS R01 DK099205NIDDK NIH HHS R01 DK101737NIDDK NIH HHS R01 DK111866
6 · The paper itself

Abstract

Hepatic fibrosis results from chronic injury and inflammation in the liver and leads to cirrhosis, liver failure, and portal hypertension. Understanding the molecular mechanisms underlying hepatic fibrosis has advanced the prospect of developing therapies for regression of the disease. Resolution of fibrosis requires a reduction of proinflammatory and fibrogenic cytokines, a decrease in extracellular matrix (ECM) protein production, an increase in collagenase activity, and finally, a disappearance of activated myofibroblasts. Exosomes are nanovesicles of endocytic origin secreted by most cell types. They epigenetically reprogram and alter the phenotype of their recipient cells and hold great promise for the reversal of fibrosis. Recent studies have shown that exosomes function as conduits for intercellular transfer and contain all the necessary components to induce resolution of fibrosis, including the ability to (1) inhibit macrophage activation and cytokine secretion, (2) remodel ECM production and decrease fibrous scars, and (3) inactivate hepatic stellate cells, a major myofibroblast population. Here, we discuss the research involving the regression of hepatic fibrosis. We focus on the newly discovered roles of exosomes during fibrogenesis and as a therapy for fibrosis reversal. We also emphasize the novel discoveries of exosome-based antifibrotic treatments

Identifiers

PMID30766956
PMCPMC6357832
OpenAlexW2905551816

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.