Evidence map›Paper›PMID 32048304›Full record

ArticleHepatology (Baltimore, Md.)2020

Deletion of Protein Kinase D3 Promotes Liver Fibrosis in Mice.

Shuya Zhang, Huan Liu, Meimei Yin, Xiuying Pei, Angelika Hausser, Eri Ishikawa, Sho Yamasaki, Zheng Gen Jin

Open access · greenAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

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  12. Loss of Protein Kinase D2 Activity Protects Against Bleomycin-Induced Dermal Fibrosis in Mice.Laboratory investigation; a journal of technical methods and pathology · 2023
    Article
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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

8 authors at 4 institutions in 4 countries.

Shuya ZhangDepartment of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY.
Huan LiuDepartment of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY.ORCID 0000-0002-2676-6982
Meimei YinDepartment of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY.
Xiuying PeiKey Laboratory of Fertility Preservation and Maintenance of Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
Angelika HausserInstitute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany.
Eri IshikawaDepartment of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Sho YamasakiDepartment of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Zheng Gen JinDepartment of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY.ORCID 0000-0002-8367-5526
Rochester Institute of Technology · USOsaka International University · JPNingxia Medical University · CNUniversity of Stuttgart · DE

Funding

SIRT6 and vascular endothelial homeostasisR01HL130167 · NHLBI · UNIVERSITY OF ROCHESTER · PI JIN, ZHENG-GEN · 2017 to 2025
$4.2M
Epigenetic regulation of vascular endothelial genes and laminar flow atheroprotectionR01HL141171 · NHLBI · UNIVERSITY OF ROCHESTER · PI JIN, ZHENG-GEN · 2019 to 2022
$1.9M
Molecular regulation of angiogenesisR01HL114570 · NHLBI · UNIVERSITY OF ROCHESTER · PI JIN, ZHENG-GEN · 2012 to 2016
$1.9M
Regulation of angiogenesis by transcription factorsR01HL128363 · NHLBI · UNIVERSITY OF ROCHESTER · PI JIN, ZHENG-GEN · 2016 to 2019
$1.5M
NHLBI NIH HHS R01 HL114570NHLBI NIH HHS R01 HL128363NHLBI NIH HHS R01 HL130167NHLBI NIH HHS R01 HL141171NIH HHS HL114570, HL128363, HL130167, HL141171
6 · The paper itself

Abstract

BACKGROUND AND

aimsLiver fibrosis (LF) is a central pathological process that occurs in most types of chronic liver diseases. Advanced LF causes cirrhosis, hepatocellular carcinoma, and liver failure. However, the exact molecular mechanisms underlying the initiation and progression of LF remain largely unknown. APPROACH AND

resultsThis study was designed to investigate the role of protein kinase D3 (PKD3; gene name Prkd3) in the regulation of liver homeostasis. We generated global Prkd3 knockout (Prkd3

conclusionsPKD3 deletion in mice drives LF through the profibrotic macrophage activation.

Indexed as

AnimalsCarbon TetrachlorideCells, CulturedDisease ProgressionHepatic Stellate CellsHumansLiverLiver CirrhosisLiver Cirrhosis, ExperimentalMacrophagesMiceMice, KnockoutMyofibroblastsPrimary Cell CultureProtein Kinase CProtein Tyrosine Phosphatase, Non-Receptor Type 6Carbon TetrachlorideProtein Kinase Cprotein kinase C nuProtein Tyrosine Phosphatase, Non-Receptor Type 6Ptpn6 protein, mouseTransforming Growth Factor beta

Identifiers

PMID32048304
PMCPMC9338785
OpenAlexW3006594468

What Socratic 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 Socratic graph.