Evidence map›Paper›PMID 32615075›Full record

ArticleThe American journal of pathology2020

Hepatic Stellate Cell-Specific Platelet-Derived Growth Factor Receptor-α Loss Reduces Fibrosis and Promotes Repair after Hepatocellular Injury.

Alexander Kikuchi, Sucha Singh, Minakshi Poddar, Toshimasa Nakao, Heidi Marie Schmidt, Jenesis D Gayden, Toshifumi Sato, Gavin E Arteel, Satdarshan P Monga

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. COX2Physiological reports · 2026
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  7. Review
  8. Roles of PDGF/PDGFR signaling in various organs.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
  9. Article
  10. Article
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  13. Review
  14. Identifying Fibrogenic Cells Following Salivary Gland Obstructive Injury.bioRxiv : the preprint server for biology · 2023
    Article
  15. Article
  16. Identifying fibrogenic cells following salivary gland obstructive injury.Frontiers in cell and developmental biology · 2023
    Article
  17. Article
  18. Article
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 1 institution in 1 country.

Alexander KikuchiDepartment of Pathology, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Sucha SinghDepartment of Pathology, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Minakshi PoddarDepartment of Pathology, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Toshimasa NakaoDepartment of Surgery, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Heidi Marie SchmidtDepartment of Pathology, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Jenesis D GaydenDepartment of Pathology, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Toshifumi SatoDepartment of Medicine, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Gavin E ArteelDepartment of Medicine, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania; Pittsburgh Liver Research Center, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Satdarshan P MongaDepartment of Pathology, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania; Department of Medicine, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania; Pittsburgh Liver Research Center, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Electronic address: smonga@pitt.edu.
University of Pittsburgh Medical Center · US

Funding

The Role of Nutrition in the Development/Progression of Alcohol-Induced Organ InjuryP50AA024337 · NIAAA · UNIVERSITY OF LOUISVILLE · PI CRAIG J. MCCLAIN · 2016 to 2026
$17.9M
Pittsburgh Liver Research CenterP30DK120531 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Shuchang Silvia Liu · 2019 to 2026
$10.9M
Biomarkers of Alcoholic HepatitisR01AA028436 · NIAAA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ARTEEL, GAVIN E, BENOS, PANAGIOTIS V · 2020 to 2024
$3.0M
Role of Platelet derived growth factor receptor-a in Liver Patho-biologyR01DK095498 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MONGA, SATDARSHAN SINGH · 2013 to 2017
$1.7M
Cell-Specific Roles of Platelet-Derived Growth Factor Receptor Alpha (PDGFRalpha) in Hepatic FibrosisF30DK107129 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KIKUCHI, ALEXANDER · 2015 to 2016
$97k
NIAAA NIH HHS P50 AA024337NIAAA NIH HHS R01 AA028436NIDDK NIH HHS F30 DK107129NIDDK NIH HHS P30 DK120531NIDDK NIH HHS R01 DK095498
6 · The paper itself

Abstract

Platelet-derived growth factor receptor (PDGFR)-α plays roles in cell survival, proliferation, and differentiation; however, its function in chronic liver injury sequelae, such as fibrosis, is unknown. Hepatic stellate cells (HSCs), the primary mediators of fibrosis, undergo activation, which entails differentiation to myofibroblasts, proliferation, migration, and collagen deposition, partially in response to PDGFs. To examine the role of PDGFR-α in HSCs, Lrat-Cre recombinase and Pdgfra-floxed mice were bred to generate Lrat-CrePdgfra-/- (knockout) animals, which were subjected to chronic liver injury through carbon tetrachloride treatment, bile duct ligation, and 0.1% 3,5-diethoxycarbonyl-1,4-dihydrocollidine. Although no major difference was observed after other types of liver injury, PDGFR-α loss in HSCs led to a significant albeit transient reduction in fibrosis after carbon tetrachloride injury, associated with increased HSC death and reduced migration. There was continued alleviation of hepatocellular injury in knockout mice despite ongoing carbon tetrachloride insult, associated with increased numbers of CD68 and F480 macrophages and increased clearance of damaged hepatocytes. Altogether our findings support a profibrotic role of PDGFR-α in HSCs during chronic liver injury in vivo via regulation of HSC survival and migration and affect the immune microenvironment, especially macrophages in clearing dying hepatocytes. Thus, our study provides a preclinical foundation for the future testing of therapeutic PDGFR-α inhibition in hepatic fibrosis, especially in combination with other therapies.

Indexed as

AnimalsCarbon TetrachlorideCarcinoma, HepatocellularCell MovementHepatic Stellate CellsLiverLiver CirrhosisLiver NeoplasmsMice, KnockoutReceptor, Platelet-Derived Growth Factor alphaReceptor Protein-Tyrosine KinasesCarbon TetrachlorideReceptor, Platelet-Derived Growth Factor alphaReceptor Protein-Tyrosine Kinases

Identifiers

PMID32615075
PMCPMC7527859
OpenAlexW3038720183

What Socratic 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 Socratic graph.