Evidence map›Paper›PMID 34202537›Full record

ReviewInternational journal of molecular sciences2021

Liver Disease: Induction, Progression, Immunological Mechanisms, and Therapeutic Interventions.

Sarah Y Neshat, Victor M Quiroz, Yuanjia Wang, Sebastian Tamayo, Joshua C Doloff

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Acute-on-chronic liver failure-associated CD45Cellular and molecular life sciences : CMLS · 2026
    Article
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  11. Observational
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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

5 authors at 2 institutions in 1 country.

Sarah Y NeshatDepartment of Biomedical Engineering, Translational Tissue Engineering Center, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.ORCID 0000-0001-7849-5603
Victor M QuirozDepartment of Biomedical Engineering, Translational Tissue Engineering Center, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.ORCID 0000-0003-0819-368X
Yuanjia WangDepartment of Biomedical Engineering, Translational Tissue Engineering Center, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Sebastian TamayoDepartment of Biomedical Engineering, Translational Tissue Engineering Center, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.ORCID 0000-0002-6099-5842
Joshua C DoloffDepartment of Biomedical Engineering, Translational Tissue Engineering Center, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Johns Hopkins University · USBloomberg (United States) · US

Funding

BIOMEDICAL ENGINEERING TRAINING PROGRAMT32GM007057 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI KANOLD, PATRICK O, KARCHIN, RACHEL · 1985 to 2023
$10.4M
HopkinsPREP: Research, Community, Professional Training and Personal GrowthR25GM109441 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI WILSON, KATHERINE L · 2015 to 2024
$3.2M
NIGMS NIH HHS R25 GM109441NIGMS NIH HHS T32 GM007057
6 · The paper itself

Abstract

The liver is an organ with impressive regenerative potential and has been shown to heal sizable portions after their removal. However, certain diseases can overstimulate its potential to self-heal and cause excessive cellular matrix and collagen buildup. Decompensation of liver fibrosis leads to cirrhosis, a buildup of fibrotic ECM that impedes the liver's ability to efficiently exchange fluid. This review summarizes the complex immunological activities in different liver diseases, and how failure to maintain liver homeostasis leads to progressive fibrotic tissue development. We also discuss a variety of pathologies that lead to liver cirrhosis, such as alcoholic liver disease and chronic hepatitis B virus (HBV). Mesenchymal stem cells are widely studied for their potential in tissue replacement and engineering. Herein, we discuss the potential of MSCs to regulate immune response and alter the disease state. Substantial efforts have been performed in preclinical animal testing, showing promising results following inhibition of host immunity. Finally, we outline the current state of clinical trials with mesenchymal stem cells and other cellular and non-cellular therapies as they relate to the detection and treatment of liver cirrhosis.

Indexed as

Disease SusceptibilityAnimalsBiomarkersCombined Modality TherapyDisease ManagementDisease ProgressionHost-Pathogen InteractionsHumansLiver DiseasesTranslational Research, BiomedicalBiomarkersalcoholic liver diseaseapoptosisautoimmune diseasecirrhosisclinical trialscytokinesfibrosishepatitishepatocyteimmunomodulationin vivolivermesenchymal stem cellsnon-alcoholic fatty liver disease

Identifiers

PMID34202537
PMCPMC8267746
OpenAlexW3177017756

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.