Evidence map›Paper›PMID 32850829›Full record

ReviewFrontiers in cell and developmental biology2020

Hepatic Stellate Cells and Hepatocarcinogenesis.

Anna E Barry, Rajkumar Baldeosingh, Ryan Lamm, Keyur Patel, Kai Zhang, Dana A Dominguez, Kayla J Kirton, Ashesh P Shah, Hien Dang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
12.9field-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

89 citing papers in PubMed, 147 citations in OpenAlex.

  1. Article
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  9. The role and mechanisms of vitamin A in suppressing hepatic stellate cell activation.Apoptosis : an international journal on programmed cell death · 2026
    Article
  10. Review
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  19. Cell-Type Deconvolution Reveals Dynamic Changes in MASLD.Liver international communications · 2025
    Article
  20. Article

29 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

9 authors at 2 institutions in 1 country.

Anna E BarryDepartment of Surgery, Thomas Jefferson University, Philadelphia, PA, United States.
Rajkumar BaldeosinghDepartment of Surgery, Thomas Jefferson University, Philadelphia, PA, United States.
Ryan LammDepartment of Surgery, Thomas Jefferson University, Philadelphia, PA, United States.
Keyur PatelDepartment of Surgery, Thomas Jefferson University, Philadelphia, PA, United States.
Kai ZhangDepartment of Surgery, Thomas Jefferson University, Philadelphia, PA, United States.
Dana A DominguezDepartment of General Surgery, UCSF East Bay, Oakland, CA, United States.
Kayla J KirtonDepartment of Surgery, Thomas Jefferson University, Philadelphia, PA, United States.
Ashesh P ShahDepartment of Surgery, Thomas Jefferson University, Philadelphia, PA, United States.
Hien DangDepartment of Surgery, Thomas Jefferson University, Philadelphia, PA, United States.
Thomas Jefferson University · USCalifornia State University, East Bay · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic stellate cells (HSCs) are a significant component of the hepatocellular carcinoma (HCC) tumor microenvironment (TME). Activated HSCs transform into myofibroblast-like cells to promote fibrosis in response to liver injury or chronic inflammation, leading to cirrhosis and HCC. The hepatic TME is comprised of cellular components, including activated HSCs, tumor-associated macrophages, endothelial cells, immune cells, and non-cellular components, such as growth factors, proteolytic enzymes and their inhibitors, and other extracellular matrix (ECM) proteins. Interactions between HCC cells and their microenvironment have become topics under active investigation. These interactions within the hepatic TME have the potential to drive carcinogenesis and create challenges in generating effective therapies. Current studies reveal potential mechanisms through which activated HSCs drive hepatocarcinogenesis utilizing matricellular proteins and paracrine crosstalk within the TME. Since activated HSCs are primary secretors of ECM proteins during liver injury and inflammation, they help promote fibrogenesis, infiltrate the HCC stroma, and contribute to HCC development. In this review, we examine several recent studies revealing the roles of HSCs and their clinical implications in the development of fibrosis and cirrhosis within the hepatic TME.

Indexed as

fibrosishepatic stellate cellshepatocellular carcinomahepatocytesinflammationtumor microenvironment

Identifiers

PMID32850829
PMCPMC7419619
OpenAlexW3047309368

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.