The DOI matches its Crossref record; 100 of the 100 references it cites were found in a registry or an index.
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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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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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Cites
Signal integration in the endoplasmic reticulum unfolded protein response
Ron, D., & Walter, P. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2199 · Cited by 6,431
β-Cell Deficit and Increased β-Cell Apoptosis in Humans With Type 2 Diabetes
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An Integrated Stress Response Regulates Amino Acid Metabolism and Resistance to Oxidative Stress
Harding, H. P., Zhang, Y., Zeng, H., Novoa, I., Lu, P. D., Calfon, M. A., Sadri, N., Yun, C., Popko, B., Paules, R. S., et al. (2003) · Molecular Cell · doi:10.1016/s1097-2765(03)00105-9 · Cited by 3,336
Urano, F., Wang, X.-Z., Bertolotti, A., Zhang, Y.-H., Chung, P., Harding, H., & Ron, D. (2000) · Science · doi:10.1126/science.287.5453.664 · Cited by 3,081
Self-citationA genome-wide association study identifies novel risk loci for type 2 diabetes
Sladek, R., Rocheleau, G., Rung, J., Dina, C., Shen, L., Serre, D., Boutin, P., Vincent, D., Belisle, A., Hadjadj, S., et al. (2007) · Nature · doi:10.1038/nature05616 · Cited by 2,993
Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels
Saxena, R., Voight, B. F., Lyssenko, V., Burtt, N. P., de Bakker, P. I. W., Chen, H., Roix, J. J., Kathiresan, S., Hirschhorn, J. N., Daly, M. J., et al. (2007) · Science · doi:10.1126/science.1142358 · Cited by 2,843
A genome-wide association study of type 2 diabetes in Finns detects multiple susceptibility variants
Scott, L. J., Mohlke, K. L., Bonnycastle, L. L., Willer, C. J., Li, Y., Duren, W. L., Erdos, M. R., Stringham, H. M., Chines, P. S., Jackson, A. U., et al. (2007) · Science · doi:10.1126/science.1142382 · Cited by 2,753
Mediators of endoplasmic reticulum stress-induced apoptosis
Szegezdi, E., Logue, S. E., Gorman, A. M., & Samali, A. (2006) · The EMBO Reports · doi:10.1038/sj.embor.7400779 · Cited by 2,345
Atomic structures of amyloid cross-β spines reveal varied steric zippers
Sawaya, M. R., Sambashivan, S., Nelson, R. A., Ivanova, M. I., Sievers, S. A., Apostol, M. I., Thompson, M. J., Balbirnie, M., Wiltzius, J. J. W., McFarlane, H. T., et al. (2007) · Nature · doi:10.1038/nature05695 · Cited by 2,279
The biology of incretin hormones
Drucker, D. J. (2006) · Cell Metabolism · doi:10.1016/j.cmet.2006.01.004 · Cited by 2,210
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The Unfolded Protein Response: From Stress Pathway to Homeostatic Regulation
Walter, P., & Ron, D. (2011) · Science · doi:10.1126/science.1209038 · Cited by 5,897
Aging and aging-related diseases: from molecular mechanisms to interventions and treatments
Guo, J., Huang, X., Dou, L., Yan, M., Shen, T., Tang, W., & Li, J. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01251-0 · Cited by 1,976
Endoplasmic Reticulum Stress and Oxidative Stress in Cell Fate Decision and Human Disease
Cao, S. S., & Kaufman, R. J. (2014) · Antioxidants and Redox Signaling · doi:10.1089/ars.2014.5851 · Cited by 1,393
A Molecular Web: Endoplasmic Reticulum Stress, Inflammation, and Oxidative Stress
Chaudhari, N., Talwar, P., Parimisetty, A., Lefebvre d’Hellencourt, C., & Ravanan, P. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00213 · Cited by 600
IRE1: ER stress sensor and cell fate executor
Chen, Y., & Brandizzí, F. (2013) · Trends in Cell Biology · doi:10.1016/j.tcb.2013.06.005 · Cited by 555
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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