Evidence map›Paper›PMID 24921008›Full record

ReviewWorld journal of biological chemistry2014

Endoglin in liver fibrogenesis: Bridging basic science and clinical practice.

Steffen K Meurer, Muhammad Alsamman, David Scholten, Ralf Weiskirchen

Open access · diamondAbstract readReview
In one paragraph

Review in World journal of biological chemistry, 2014. 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
1.8field-weighted citation impact, top 15% 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, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. CD105: tumor diagnosis, prognostic marker and future tumor therapeutic target.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  5. Review
  6. Endoglin in the Spotlight to Treat Cancer.International journal of molecular sciences · 2021
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Endoglin in human liver disease and murine models of liver fibrosis-A protective factor against liver fibrosis.Liver international : official journal of the International Association for the Study of the Liver · 2018
    Article
  15. Article
  16. Article
  17. Review
  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

4 authors at 1 institution in 1 country.

Steffen K MeurerSteffen K Meurer, Ralf Weiskirchen, Institute of Clinical Chemistry and Pathobiochemistry, RWTH University Hospital Aachen, D-52074 Aachen, Germany.
Muhammad AlsammanSteffen K Meurer, Ralf Weiskirchen, Institute of Clinical Chemistry and Pathobiochemistry, RWTH University Hospital Aachen, D-52074 Aachen, Germany.
David ScholtenSteffen K Meurer, Ralf Weiskirchen, Institute of Clinical Chemistry and Pathobiochemistry, RWTH University Hospital Aachen, D-52074 Aachen, Germany.
Ralf WeiskirchenSteffen K Meurer, Ralf Weiskirchen, Institute of Clinical Chemistry and Pathobiochemistry, RWTH University Hospital Aachen, D-52074 Aachen, Germany.
RWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoglin, also known as cluster of differentiation CD105, was originally identified 25 years ago as a novel marker of endothelial cells. Later it was shown that endoglin is also expressed in pro-fibrogenic cells including mesangial cells, cardiac and scleroderma fibroblasts, and hepatic stellate cells. It is an integral membrane-bound disulfide-linked 180 kDa homodimeric receptor that acts as a transforming growth factor-β (TGF-β) auxiliary co-receptor. In humans, several hundreds of mutations of the endoglin gene are known that give rise to an autosomal dominant bleeding disorder that is characterized by localized angiodysplasia and arteriovenous malformation. This disease is termed hereditary hemorrhagic telangiectasia type I and induces various vascular lesions, mainly on the face, lips, hands and gastrointestinal mucosa. Two variants of endoglin (i.e., S- and L-endoglin) are formed by alternative splicing that distinguishes from each other in the length of their cytoplasmic tails. Moreover, a soluble form of endoglin, i.e., sol-Eng, is shedded by the matrix metalloprotease-14 that cleaves within the extracellular juxtamembrane region. Endoglin interacts with the TGF-β signaling receptors and influences Smad-dependent and -independent effects. Recent work has demonstrated that endoglin is a crucial mediator during liver fibrogenesis that critically controls the activity of the different Smad branches. In the present review, we summarize the present knowledge of endoglin expression and function, its involvement in fibrogenic Smad signaling, current models to investigate endoglin function, and the diagnostic value of endoglin in liver disease.

Indexed as

Bleeding disordersDiseaseSignallingTelangiectasiaTransforming growth factor-β

Identifiers

PMID24921008
PMCPMC4050112
OpenAlexW1732498503

What OpenQuestion 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 OpenQuestion graph.