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Pharmacological targeting of endoplasmic reticulum stress in pancreatic beta cells.
Trends Pharmacol. Sci. 42, 85-95 (2021)
Diabetes is a disease with pandemic dimensions and no pharmacological treatment prevents disease progression. Dedifferentiation has been proposed to be a driver of beta-cell dysfunction in both type 1 and type 2 diabetes. Regenerative therapies aim to re-establish function in dysfunctional or dedifferentiated beta cells and restore the defective insulin secretion. Unsustainable levels of insulin production, with increased demand at disease onset, strain the beta-cell secretory machinery, leading to endoplasmic reticulum (ER) stress. Unresolved chronic ER stress is a major contributor to beta-cell loss of function and identity. Restoring ER homeostasis, enhancing ER-associated degradation of misfolded protein, and boosting chaperoning activity, are emerging therapeutic approaches for diabetes treatment.
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Publication type
Article: Journal article
Document type
Review
Keywords
Beta Cell ; Diabetes ; Endoplasmic Reticulum Stress ; Pharmacology; Unfolded Protein Response; Thioredoxin-interacting Protein; Er Stress; Gene-expression; Allosteric Inhibition; Misfolded Proinsulin; Insulin Production; Quality-control; Dedifferentiation; Ire1-alpha
ISSN (print) / ISBN
0165-6147
e-ISSN
1873-3735
Quellenangaben
Volume: 42,
Issue: 2,
Pages: 85-95
Publisher
Cell Press
Publishing Place
Amsterdam
Non-patent literature
Publications
Reviewing status
Peer reviewed