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Pancreatic β-cell identity in diabetes
Open accessAbstract
Recovery of functional β‐cell mass continues to be an ongoing challenge in treating diabetes. Initial work studying β‐cells suggested apoptotic β‐cell death as a main contributor for the loss of β‐cell mass in diabetes. Restoration of β‐cells either by transplant or stimulating proliferation of remaining β‐cells or precursors would then logically be a viable therapeutic option for diabetes. However, recent work has highlighted the inherent β‐cell plasticity and the critical role of loss of β‐cell identity in diabetes, and has suggested that β‐cells fail to maintain a fully differentiated glucose‐responsive and drug‐responsive state, particularly in diabetic individuals with poorly controlled, long‐lasting periods of hyperglycaemia. Understanding the underlying mechanisms of loss of β‐cell identity and conversion in other cell types, as well as how to regain their mature differentiated functional state, is critical to develop novel therapeutic strategies to prevent or reverse these processes. In this review, we discuss the role of plasticity and loss of β‐cell identity in diabetes, the current understanding of mechanisms involved in altering this mature functional β‐cell state and potential progresses to identify novel therapeutic targets providing better opportunities for slowing or preventing diabetes progression.
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“Recent data have identified β-cell dedifferentiation, loss of identity, or reversion to a progenitor-like state, as a compensatory response to islet inflammatory stress, with evidence of β-cell dedifferentiation in models of T1D and T2D [35].”
From β-Cell pre-mir-21 induces dysfunction and loss of cellular identity by targeting transforming growth factor beta 2 (Tgfb2) and Smad family member 2 (Smad2) mRNAs (2021) · cites this paper as [35]
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Metadata
- Authors
- Remedi, M. S., & Emfinger, C.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Remedi, M. S.
- Venue
- Diabetes, Obesity and Metabolism
- Publisher
- Wiley
- Published
- 2016-09
- Volume
- 18
- Issue
- S1
- Pages
- 110-116
- ISSN
- 1462-8902 (ISSN-L)
- 1463-1326
- PMC
- PMC5021188
- OpenAlex
- W2518974058
- Cited by
- 128
- References
- 80
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 15 · 2023: 16 · 2022: 26 · 2021: 25 · 2020: 11 · 2019: 12 · 2018: 5 · 2017: 5 · 2016: 1
- FWCI
- 1.52
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Diabetes Obesity and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01 DK098584)
- Diabetes Research Center (5P60 DK020579)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- beta cell plasticity, beta cell differentiation, beta-cell mass loss, beta-cell apoptosis, hyperglycemia, glucose responsiveness, drug response, diabetes treatment, beta cell regeneration
- MeSH terms
- Cell Plasticity, Insulin Secretion, Animals, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Humans, Hypoglycemic Agents, Insulin, Regeneration, Disease Progression, Cell Proliferation, Insulin-Secreting Cells, Mice, Cell Dedifferentiation, Cell Transdifferentiation
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