Evidence map›Paper›PMID 36711019›Full record

ReviewFrontiers in physiology2023

"iPSC-derived liver organoids and inherited bleeding disorders: Potential and future perspectives".

Giacomo Roman, Benedicte Stavik, Knut H Lauritzen, Per Morten Sandset, Sean P Harrison, Gareth J Sullivan, Maria Eugenia Chollet

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

7 authors at 2 institutions in 1 country.

Giacomo RomanDepartment of Hematology, Oslo University Hospital, Oslo, Norway.
Benedicte StavikDepartment of Hematology, Oslo University Hospital, Oslo, Norway.
Knut H LauritzenDepartment of Hematology, Oslo University Hospital, Oslo, Norway.
Per Morten SandsetDepartment of Hematology, Oslo University Hospital, Oslo, Norway.
Sean P HarrisonDepartment of Pediatric Research, Oslo University Hospital, Oslo, Norway.
Gareth J SullivanDepartment of Pediatric Research, Oslo University Hospital, Oslo, Norway.
Maria Eugenia CholletDepartment of Hematology, Oslo University Hospital, Oslo, Norway.
Oslo University Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The bleeding phenotype of hereditary coagulation disorders is caused by the low or undetectable activity of the proteins involved in hemostasis, due to a broad spectrum of genetic alterations. Most of the affected coagulation factors are produced in the liver. Therefore, two-dimensional (2D) cultures of primary human hepatocytes and recombinant overexpression of the factors in non-human cell lines have been primarily used to mimic disease pathogenesis and as a model for innovative therapeutic strategies. However, neither human nor animal cells fully represent the hepatocellular biology and do not harbor the exact genetic background of the patient. As a result, the inability of the current

Indexed as

bleeding disorderscell therapycoagulation factor deficienciesCRISPRdisease modelinggenome editinginduced pluripotent stem cellsliver organoids

Identifiers

PMID36711019
PMCPMC9880334
OpenAlexW4315797496

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.