ReviewMolecular metabolism2021
An accomplice more than a mere victim: The impact of β-cell ER stress on type 1 diabetes pathogenesis.
Review in Molecular metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 71 citations in OpenAlex.
- Deletion of the T1D risk geneBiochemistry and biophysics reports · 2026Article
- The central role of the β-cell in diabetes: from monogenic forms to type 1, type 2, and gestational diabetes.Reviews in endocrine & metabolic disorders · 2026Review
- 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
- Beyond Sequence: Posttranslational Remodeling of Antigens in Autoimmunity.Immunological reviews · 2026Review
- The bile acid-sensive ion channel (BASIC) is expressed in pancreatic α-cells and involved in glucagon secretion.Pflugers Archiv : European journal of physiology · 2026Review
- A spatial atlas of pancreatic remodelling in type 1 diabetes.Nature metabolism · 2026Article
- Toward Personalized Medicine in Type 1 Diabetes: Understanding How Patient Heterogeneity Influences Therapeutic Efficacy.Diabetes, obesity & metabolism · 2026Review
- Transient ER stress cell-autonomously promotes beta cell cycling in mice.Diabetologia · 2026Article
- A microenvironment-driven HLA-II-associated insulin neoantigen elicits persistent memory T cell activation in diabetes.Nature immunology · 2026Article
- Emerging insights of decoding the genetic blueprint, molecular mechanisms, and future horizons in precision medicine for the treatment of type 2 diabetes.Journal of diabetes and metabolic disorders · 2025Review
- Defining the role of β-cell IRE1α/XBP1 pathway and its gene regulatory network components in non-obese diabetic mice.Nature communications · 2025Article
- Beta cell dysfunction occurs independently of insulitis in type 1 diabetes pathogenesis.Cell reports · 2025Article
- Autoreactive T Cells and Cytokine Stress Drive β-Cell Senescence Entry and Accumulation in Type 1 Diabetes.Diabetes · 2025Article
- Diabetes mellitus and the key role of endoplasmic reticulum stress in pancreatic β cells.Nature reviews. Endocrinology · 2025Review
- Association between atherogenic index of plasma and risk of type 2 diabetes mellitus and the mediating effect of BMI: a comparative analysis in Chinese and Japanese populations.Diabetology & metabolic syndrome · 2025Article
- Pancreatic exocrine damage induces beta cell stress in zebrafish larvae.Diabetologia · 2025Article
- A plasma metabolomic analysis revealed the metabolic regulatory mechanism of the water extract of Dendrobium huoshanense in improving streptozotocin-induced type 1 diabetes model rats.Journal of natural medicines · 2025Article
- microRNAs in Type 1 Diabetes: Roles, Pathological Mechanisms, and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Mettl3 deficiency leads to impaired insulin secretion via regulating Ire1a of mature β-cells in mice.Scientific reports · 2025Article
- Disease-modifying pharmacological treatments of type 1 diabetes: Molecular mechanisms, target checkpoints, and possible combinatorial treatments.Pharmacological reviews · 2025Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPancreatic β-cells are the insulin factory of an organism with a mission to regulate glucose homeostasis in the body. Due to their high secretory activity, β-cells rely on a functional and intact endoplasmic reticulum (ER). Perturbations to ER homeostasis and unmitigated stress lead to β-cell dysfunction and death. Type 1 diabetes (T1D) is a chronic inflammatory disease caused by the autoimmune-mediated destruction of β-cells. Although autoimmunity is an essential component of T1D pathogenesis, accumulating evidence suggests an important role of β-cell ER stress and aberrant unfolded protein response (UPR) in disease initiation and progression. SCOPE OF REVIEW: In this article, we introduce ER stress and the UPR, review β-cell ER stress in various mouse models, evaluate its involvement in inflammation, and discuss the effects of ER stress on β-cell plasticity and demise, and islet autoimmunity in T1D. We also highlight the relationship of ER stress with other stress response pathways and provide insight into ongoing clinical studies targeting ER stress and the UPR for the prevention or treatment of T1D. MAJOR
conclusionsEvidence from ex vivo studies, in vivo mouse models, and tissue samples from patients suggest that β-cell ER stress and a defective UPR contribute to T1D pathogenesis. Thus, restoration of β-cell ER homeostasis at various stages of disease presents a plausible therapeutic strategy for T1D. Identifying the specific functions and regulation of each UPR sensor in β-cells and uncovering the crosstalk between stressed β-cells and immune cells during T1D progression would provide a better understanding of the molecular mechanisms of disease process, and may reveal novel targets for development of effective therapies for T1D.
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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 Socratic graph.