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Transcription factors that shape the mammalian pancreas

Authors
  • Jennings, Rachel E.1, 2
  • Scharfmann, Raphael3
  • Staels, Willem3, 4, 5
  • 1 University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK , Manchester (United Kingdom)
  • 2 Manchester University NHS Foundation Trust, Manchester, UK , Manchester (United Kingdom)
  • 3 Université de Paris, Paris, 75014, France , Paris (France)
  • 4 Vrije Universiteit Brussel, Laarbeeklaan 103, Brussels, 1090, Belgium , Brussels (Belgium)
  • 5 University Hospital of Brussels, Jette, Belgium , Jette (Belgium)
Type
Published Article
Journal
Diabetologia
Publisher
Springer-Verlag
Publication Date
Sep 07, 2020
Volume
63
Issue
10
Pages
1974–1980
Identifiers
DOI: 10.1007/s00125-020-05161-0
Source
Springer Nature
Keywords
License
Green

Abstract

Improving our understanding of mammalian pancreas development is crucial for the development of more effective cellular therapies for diabetes. Most of what we know about mammalian pancreas development stems from mouse genetics. We have learnt that a unique set of transcription factors controls endocrine and exocrine cell differentiation. Transgenic mouse models have been instrumental in studying the function of these transcription factors. Mouse and human pancreas development are very similar in many respects, but the devil is in the detail. To unravel human pancreas development in greater detail, in vitro cellular models (including directed differentiation of stem cells, human beta cell lines and human pancreatic organoids) are used; however, in vivo validation of these results is still needed. The current best ‘model’ for studying human pancreas development are individuals with monogenic forms of diabetes. In this review, we discuss mammalian pancreas development, highlight some discrepancies between mouse and human, and discuss selected transcription factors that, when mutated, cause permanent neonatal diabetes. Graphical abstract

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