Evidence map›Paper›PMID 31161346›Full record

ReviewDiabetologia2019

Genome editing of human pancreatic beta cell models: problems, possibilities and outlook.

Diego Balboa, Rashmi B Prasad, Leif Groop, Timo Otonkoski

Abstract readReview
In one paragraph

Review in Diabetologia, 2019. 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
–field-weighted citation impact
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.

  1. Review
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  10. Genome engineering and disease modelingWorld journal of stem cells · 2021
    Review
  11. Article
  12. Modeling different types of diabetes using human pluripotent stem cells.Cellular and molecular life sciences : CMLS · 2021
    Review
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  15. 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

4 authors.

Diego BalboaStem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, PO Box 63, (Haartmaninkatu 8), FI-00014, Helsinki, Finland.
Rashmi B PrasadGenomics, Diabetes and Endocrinology, Lund University Diabetes Centre, CRC, Malmö, Sweden.
Leif GroopGenomics, Diabetes and Endocrinology, Lund University Diabetes Centre, CRC, Malmö, Sweden.
Timo OtonkoskiStem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, PO Box 63, (Haartmaninkatu 8), FI-00014, Helsinki, Finland. timo.otonkoski@helsinki.fi.ORCID 0000-0001-9190-2496

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding the molecular mechanisms behind beta cell dysfunction is essential for the development of effective and specific approaches for diabetes care and prevention. Physiological human beta cell models are needed for this work. We review the possibilities and limitations of currently available human beta cell models and how they can be dramatically enhanced using genome-editing technologies. In addition to the gold standard, primary isolated islets, other models now include immortalised human beta cell lines and pluripotent stem cell-derived islet-like cells. The scarcity of human primary islet samples limits their use, but valuable gene expression and functional data from large collections of human islets have been made available to the scientific community. The possibilities for studying beta cell physiology using immortalised human beta cell lines and stem cell-derived islets are rapidly evolving. However, the functional immaturity of these cells is still a significant limitation. CRISPR-Cas9 (Clustered Regularly Interspaced Short Palindromic Repeats/CRISPR-associated protein 9) has enabled precise engineering of specific genetic variants, targeted transcriptional modulation and genome-wide genetic screening. These approaches can now be exploited to gain understanding of the mechanisms behind coding and non-coding diabetes-associated genetic variants, allowing more precise evaluation of their contribution to diabetes pathogenesis. Despite all the progress, genome editing in primary pancreatic islets remains difficult to achieve, an important limitation requiring further technological development.

Indexed as

Gene EditingGenome, HumanClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsDiabetes MellitusGene SilencingGenetic VariationGenotypeHumansInsulin-Secreting CellsPluripotent Stem CellsPolymorphism, Single NucleotideRiskBeta cellsCell modelsCRISPR-Cas9DiabetesGenome editingHuman isletsPancreasReviewStem cells

Identifiers

PMID31161346
PMCPMC6647170

What OpenQuestion holds

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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.