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Endoplasmic reticulum stress and pancreatic β-cell death
Open accessAbstract
In pancreatic β-cells, the endoplasmic reticulum (ER) is an important cellular compartment for insulin biosynthesis, which accounts for half of the total protein production in these cells. Protein flux through the ER must be carefully monitored to prevent dysregulation of ER homeostasis and stress. ER stress elicits a signaling cascade known as the unfolded protein response (UPR), which influences both life and death decisions in cells. β-cell loss is a pathological component of both type 1 and type 2 diabetes, and recent findings suggest that ER stress is involved. In this review, we address the transition from the physiological ER stress response to the pathological response, and explore the mechanisms of ER stress-mediated β-cell loss during the progression of diabetes.
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“Over time, both mechanisms, recurrent postprandial hyperglycemia and prolonged insulin secretion, may promote β-cell stress and accelerate progression from impaired glucose tolerance to overt T2D (34,35).”
From Melatonin Impairs Glucose Tolerance, First-Phase Insulin Secretion, and Insulin Feedback Inhibition; Interaction With MTNR1B Diabetes Risk Variant (2026) · cites this paper as [34]
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“Accordingly, elevated melatonin in the presence of food intake may represent an additional path to prolonged insulin secretion, which may cause endoplasmic reticulum stress in β-cells and ultimately lead to β-cell failure (34).”
From Melatonin Impairs Glucose Tolerance, First-Phase Insulin Secretion, and Insulin Feedback Inhibition; Interaction With MTNR1B Diabetes Risk Variant (2026) · cites this paper as [34]
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“Inflammatory cytokines, hypoxia, and hyperglycemia can all induce an ER stress response in β cells that leads to cell dysfunction and apoptosis.”
From Developments in stem cell-derived islet replacement therapy for treating type 1 diabetes (2023) · cites this paper as [127]
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“Perturbations in normal metabolism and environmental conditions can induce endoplasmic reticulum (ER) stress and initiate the unfolded protein response (UPR).”
From Developments in stem cell-derived islet replacement therapy for treating type 1 diabetes (2023) · cites this paper as [127]
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“While this pathway aims to restore protein homeostasis under mild stress conditions, it will induce apoptosis if the trigger is more severe.”
From Developments in stem cell-derived islet replacement therapy for treating type 1 diabetes (2023) · cites this paper as [127]
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Metadata
- Authors
- Fonseca, S. G., Gromada, J., & Urano, F.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2011-03
- Volume
- 22
- Issue
- 7
- Pages
- 266-74
- ISSN
- 1043-2760 (ISSN-L)
- PMC
- PMC3130122
- OpenAlex
- W2039420809
- Cited by
- 384
- References
- 100
- Citations by year
- 2026: 7 · 2025: 14 · 2024: 20 · 2023: 30 · 2022: 34 · 2021: 34 · 2020: 28 · 2019: 35 · 2018: 18 · 2017: 31 · 2016: 23 · 2015: 27 · 2014: 32 · 2013: 21 · 2012: 24
- FWCI
- 2.26
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK067493, 5 P30 DK 32520, P30DK032520)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Keywords
- endoplasmic reticulum stress, pancreatic beta cells, beta-cell death, unfolded protein response, insulin biosynthesis, type 1 diabetes, type 2 diabetes, ER homeostasis, diabetes pathogenesis
- MeSH terms
- Animals, Diabetes Mellitus, Endoplasmic Reticulum, Humans, Stress, Physiological, Protein Biosynthesis, Cell Death, Oxidative Stress, Disease Progression, Insulin-Secreting Cells, Unfolded Protein Response, Molecular Targeted Therapy
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