ArticleIslets2014
From immunobiology to β-cell biology: the changing perspective on type 1 diabetes.
Article in Islets, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Proinflammatory signaling in islet β cells propagates invasion of pathogenic immune cells in autoimmune diabetes.Cell reports · 2022Article
- Regulation of Tissue Inflammation by 12-Lipoxygenases.Biomolecules · 2021Review
- Beta Cell Dedifferentiation Induced by IRE1α Deletion Prevents Type 1 Diabetes.Cell metabolism · 2020Article
- Role of the 12-lipoxygenase pathway in diabetes pathogenesis and complications.Pharmacology & therapeutics · 2019Review
- The Bile Acid TUDCA Improves Beta-Cell Mass and Reduces Insulin Degradation in Mice With Early-Stage of Type-1 Diabetes.Frontiers in physiology · 2019Article
- Redox-Sensitive Innate Immune Pathways During Macrophage Activation in Type 1 Diabetes.Antioxidants & redox signaling · 2018Review
- An immunohistochemical study of nitrotyrosine expression in pancreatic islets of cases with increasing duration of type 1 diabetes and without diabetes.Histochemistry and cell biology · 2017Article
- Development of the Nonobese Diabetic Mouse and Contribution of Animal Models for Understanding Type 1 Diabetes.Pancreas · 2017Review
- Measurement of Differentially Methylated INS DNA Species in Human Serum Samples as a Biomarker of Islet β Cell Death.Journal of visualized experiments : JoVE · 2016Article
- Peroxisome Proliferator-activated Receptor-γ Activation Augments the β-Cell Unfolded Protein Response and Rescues Early Glycemic Deterioration and β Cell Death in Non-obese Diabetic Mice.The Journal of biological chemistry · 2016Article
- Biomarkers of β-Cell Stress and Death in Type 1 Diabetes.Current diabetes reports · 2016Review
- Nucleic acid biomarkers of β cell stress and death in type 1 diabetes.Current opinion in endocrinology, diabetes, and obesity · 2016Review
- Considerations for Defining Cytokine Dose, Duration, and Milieu That Are Appropriate for Modeling Chronic Low-Grade Inflammation in Type 2 Diabetes.Journal of diabetes research · 2016Review
- Article
- Minireview: 12-Lipoxygenase and Islet β-Cell Dysfunction in Diabetes.Molecular endocrinology (Baltimore, Md.) · 2015Review
- Proinsulin misfolding and endoplasmic reticulum stress during the development and progression of diabetes.Molecular aspects of medicine · 2015Review
- Maintenance of Pdx1 mRNA translation in islet β-cells during the unfolded protein response.Molecular endocrinology (Baltimore, Md.) · 2014Article
Corrections and comments
- Comment on
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Type 1 Diabetes (T1D) is characterized by the immune mediated destruction of β cells. Clinical studies have focused on drug therapies to modulate autoimmunity, yet none of these interventions has resulted in durable preservation of β-cell function. These findings raise the possibility that initiating or propagating events outside of the immune system should be considered in future efforts to prevent or reverse T1D. An emerging concept suggests that defects inherent to the β cell may trigger autoimmunity. A study by Engin et al. in type 1 diabetic NOD mice suggests that excessive β-cell endoplasmic reticulum stress arising from environmental insults results in abnormal protein synthesis, folding, and/or processing. Administration of the chemical protein folding chaperone TUDCA resulted in recovery of β-cell endoplasmic reticulum function and a diminished incidence of diabetes in NOD mice. We propose here that these data and others support a model whereby an inadequate or defective β-cell endoplasmic reticulum response results in the release of β-cell antigens and neoantigens that initiate autoimmunity. Pharmacologic therapies that either mitigate these early β-cell stressors or enhance the ability of β cells to cope with such stressors may prove to be effective in the prevention or treatment of T1D.
Indexed as
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What OpenQuestion holds
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.