Evidence map›Paper›PMID 28293634›Full record

ReviewBioMed research international2017

SECs (Sinusoidal Endothelial Cells), Liver Microenvironment, and Fibrosis.

Vaishaali Natarajan, Edward N Harris, Srivatsan Kidambi

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in BioMed research international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.2field-weighted citation impact, top 5% 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, 81 citations in OpenAlex.

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  14. Radiation-induced liver disease: beyond DNA damage.Cell cycle (Georgetown, Tex.) · 2023
    Review
  15. Customized liver organoids as an advancedInternational journal of biological sciences · 2023
    Review
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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

3 authors at 1 institution in 1 country.

Vaishaali NatarajanDepartment of Chemical and Biomolecular Engineering, University of Nebraska, Lincoln, NE, USA.
Edward N HarrisDepartment of Biochemistry, University of Nebraska, Lincoln, NE, USA; Nebraska Center for Integrated Biomolecular Communication, University of Nebraska, Lincoln, NE, USA; Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA; Nebraska Center for the Prevention of Obesity Diseases, University of Nebraska, Lincoln, NE, USA.
Srivatsan KidambiDepartment of Chemical and Biomolecular Engineering, University of Nebraska, Lincoln, NE, USA; Nebraska Center for Integrated Biomolecular Communication, University of Nebraska, Lincoln, NE, USA; Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA; Nebraska Center for the Prevention of Obesity Diseases, University of Nebraska, Lincoln, NE, USA; Nebraska Center for Materials and Nanoscience, University of Nebraska, Lincoln, NE, USA; Mary and Dick Holland Regenerative Medicine Program, University of Nebraska Medical Center, Omaha, NE, USA.ORCID 0000-0002-0282-0411
University of Nebraska–Lincoln · US

Funding

The role of stress in the fetal origin of obesity and metabolic dysfunctionP20GM104320 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI ZEMPLENI, JANOS · 2014 to 2024
$24.9M
Targeted mass spectrometry approaches to understand CART processing and recepter interactionsP20GM113126 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI RAZAVI RIZI, MOHAMMAD · 2016 to 2025
$20.8M
Liver-Mediated Clearance of Low Molecular Weight HeparinsR01HL130864 · NHLBI · UNIVERSITY OF NEBRASKA LINCOLN · PI HARRIS, EDWARD N · 2016 to 2019
$1.6M
NHLBI NIH HHS R01 HL130864NIGMS NIH HHS P20 GM104320NIGMS NIH HHS P20 GM113126
6 · The paper itself

Abstract

Liver fibrosis is a wound-healing response to chronic liver injury such as alcoholic/nonalcoholic fatty liver disease and viral hepatitis with no FDA-approved treatments. Liver fibrosis results in a continual accumulation of extracellular matrix (ECM) proteins and paves the way for replacement of parenchyma with nonfunctional scar tissue. The fibrotic condition results in drastic changes in the local mechanical, chemical, and biological microenvironment of the tissue. Liver parenchyma is supported by an efficient network of vasculature lined by liver sinusoidal endothelial cells (LSECs). These nonparenchymal cells are highly specialized resident endothelial cell type with characteristic morphological and functional features. Alterations in LSECs phenotype including lack of LSEC fenestration, capillarization, and formation of an organized basement membrane have been shown to precede fibrosis and promote hepatic stellate cell activation. Here, we review the interplay of LSECs with the dynamic changes in the fibrotic liver microenvironment such as matrix rigidity, altered ECM protein profile, and cell-cell interactions to provide insight into the pivotal changes in LSEC physiology and the extent to which it mediates the progression of liver fibrosis. Establishing the molecular aspects of LSECs in the light of fibrotic microenvironment is valuable towards development of novel therapeutic and diagnostic targets of liver fibrosis.

Indexed as

AnimalsEndothelial CellsExtracellular MatrixHepatic Stellate CellsHepatocytesHumansLiverLiver CirrhosisPhenotype

Identifiers

PMID28293634
PMCPMC5331310
OpenAlexW2587892042

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.