Evidence map›Paper›PMID 31671683›Full record

ReviewInternational journal of molecular sciences2019

β-Cell Maturation and Identity in Health and Disease.

Ciro Salinno, Perla Cota, Aimée Bastidas-Ponce, Marta Tarquis-Medina, Heiko Lickert, Mostafa Bakhti

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
–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

47 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Postnatal refinement of CaChannels (Austin, Tex.) · 2026
    Article
  3. Review
  4. Undernutrition-related diabetes in mice is linked to early undernutrition.American journal of physiology. Endocrinology and metabolism · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Ppid is necessary for overnutrition-induced β-cell loss.American journal of physiology. Endocrinology and metabolism · 2026
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Advanced therapy to cure diabetes: mission impossible is now possible?Frontiers in cell and developmental biology · 2024
    Review
  20. Differential CpG methylation atbioRxiv : the preprint server for biology · 2023
    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

6 authors.

Ciro SalinnoInstitute of Diabetes and Regeneration Research, Helmholtz Zentrum München, D-85764 Neuherberg, Germany. ciro.salinno@helmholtz-muenchen.de.
Perla CotaInstitute of Diabetes and Regeneration Research, Helmholtz Zentrum München, D-85764 Neuherberg, Germany. perla.cota@helmholtz-muenchen.de.
Aimée Bastidas-PonceInstitute of Diabetes and Regeneration Research, Helmholtz Zentrum München, D-85764 Neuherberg, Germany. aimee.bastidas-ponce@helmholtz-muenchen.de.
Marta Tarquis-MedinaInstitute of Diabetes and Regeneration Research, Helmholtz Zentrum München, D-85764 Neuherberg, Germany. marta.medina@helmholtz-muenchen.de.
Heiko LickertInstitute of Diabetes and Regeneration Research, Helmholtz Zentrum München, D-85764 Neuherberg, Germany. heiko.lickert@helmholtz-muenchen.de.
Mostafa BakhtiInstitute of Diabetes and Regeneration Research, Helmholtz Zentrum München, D-85764 Neuherberg, Germany. mostafa.bakhti@helmholtz-muenchen.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The exponential increase of patients with diabetes mellitus urges for novel therapeutic strategies to reduce the socioeconomic burden of this disease. The loss or dysfunction of insulin-producing β-cells, in patients with type 1 and type 2 diabetes respectively, put these cells at the center of the disease initiation and progression. Therefore, major efforts have been taken to restore the β-cell mass by cell-replacement or regeneration approaches. Implementing novel therapies requires deciphering the developmental mechanisms that generate β-cells and determine the acquisition of their physiological phenotype. In this review, we summarize the current understanding of the mechanisms that coordinate the postnatal maturation of β-cells and define their functional identity. Furthermore, we discuss different routes by which β-cells lose their features and functionality in type 1 and 2 diabetic conditions. We then focus on potential mechanisms to restore the functionality of those β-cell populations that have lost their functional phenotype. Finally, we discuss the recent progress and remaining challenges facing the generation of functional mature β-cells from stem cells for cell-replacement therapy for diabetes treatment.

Indexed as

Cell DifferentiationCell TransdifferentiationDiabetes MellitusDisease ProgressionHumansInsulin-Secreting CellsPhenotypeSignal TransductiondedifferentiationdiabetesdysfunctionidentitymaturationpostnatalSC-β-cellssenescencetransdifferentiationβ-cell

Identifiers

PMID31671683
PMCPMC6861993

What Socratic 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 Socratic graph.