ReviewJournal of investigative medicine : the official publication of the American Federation for Clinical Research2016
ER stress and development of type 1 diabetes.
Review in Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 79 citations in OpenAlex.
- Association of NF-E2 Related Factor 2 (Nrf2) and inflammatory cytokines in recent onset Type 2 Diabetes Mellitus.Scientific reports · 2018Trial
- Deletion of the T1D risk geneBiochemistry and biophysics reports · 2026Article
- GLP1-E2 therapy delays autoimmune diabetes in late-stage prediabetic NOD mice and potentiates low-dose anti-CD3 therapy for enhanced disease protection.Diabetologia · 2026Article
- Pancreatic β-cell aging in physiology and diabetes: emerging roles of m6A mRNA methylation.Journal of molecular endocrinology · 2026Review
- Beyond bystanders: How β cell stress shapes the autoimmune response in T1D.Science translational medicine · 2026Review
- Defining the role of β-cell IRE1α/XBP1 pathway and its gene regulatory network components in non-obese diabetic mice.Nature communications · 2025Article
- A Small-Molecule Mitofusin 1 Agonist Enhances Islet Survival Under Hypoxic Conditions In Vitro and Improves Transplantation Outcomes.Biomolecules · 2025Article
- Molecular and Inflammatory Etiologies of β-Cell Dysfunction in Type 1 Diabetes.Physiology (Bethesda, Md.) · 2025Review
- Possible Involvement of X-Box Binding Protein-1 in the Onset of Pulpitis.European endodontic journal · 2024Article
- Inhibition of PERK-mediated unfolded protein response acts as a switch for reversal of residual senescence and as senolytic therapy in glioblastoma.Neuro-oncology · 2024Article
- Chrysin reduces heart endoplasmic reticulum stress-induced apoptosis by inhibiting PERK and Caspase 3-7 in high-fat diet-fed rats.Molecular biology reports · 2024Article
- A Translational Regulatory Mechanism Mediated by Hypusinated Eukaryotic Initiation Factor 5A Facilitates β-Cell Identity and Function.Diabetes · 2024Article
- Stress-induced β cell early senescence confers protection against type 1 diabetes.Cell metabolism · 2023Article
- Islet graft function by mixed meal tolerance testing is sustained over 4 years in young children undergoing total pancreatectomy with islet autotransplantation.Clinical transplantation · 2023Article
- Effects of multiple stressors on pancreatic human islets proteome reveal new insights into the pathways involved.Proteomics · 2023Article
- Linkage analysis using whole exome sequencing data implicates SLC17A1, SLC17A3, TATDN2 and TMEM131L in type 1 diabetes in Kuwaiti families.Scientific reports · 2023Article
- SGLT1/2 inhibition improves glycemic control and multi-organ protection in type 1 diabetes.iScience · 2023Article
- Bone and the Unfolded Protein Response: In Sickness and in Health.Calcified tissue international · 2023Review
- Type 1Micromachines · 2023Review
- Endoplasmic reticulum homeostasis: a potential target for diabetic nephropathy.Frontiers in endocrinology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Type 1 diabetes (T1D) results from an autoimmune-mediated destruction of pancreatic β cells. The incidence of T1D is on the rise globally around 3% to 5% per year and rapidly increasing incidence in younger children is of the greatest concern. currently, there is no way to cure or prevent T1D; hence, a deeper understanding of the underlying molecular mechanisms of this disease is essential to the development of new effective therapies. The endoplasmic reticulum (ER) is an organelle with multiple functions that are essential for cellular homeostasis. Excessive demand on the ER, chronic inflammation, and environmental factors lead to ER stress and to re-establish cellular homeostasis, the adaptive unfolded protein response (UPR) is triggered. However, chronic ER stress leads to a switch from a prosurvival to a proapoptotic UPR, resulting in cell death. Accumulating data have implicated ER stress and defective UPR in the pathogenesis of inflammatory and autoimmune diseases, and ER stress has been implicated in β-cell failure in type 2 diabetes. However, the role of ER stress and the UPR in β-cell pathophysiology and in the initiation and propagation of the autoimmune responses in T1D remains undefined. This review will highlight the current understanding and recent in vivo data on the role of ER stress and adaptive responses in T1D pathogenesis and the potential therapeutic aspect of enhancing β-cell ER function and restoring UPR defects as novel clinical strategies against this disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.