ReviewAnnual review of biochemistry2012
Endoplasmic reticulum stress and type 2 diabetes.
Review in Annual review of biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 327 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
327 citing papers in PubMed, 1 synthesis or guideline pooled it, 599 citations in OpenAlex.
- Endoplasmic Reticulum Stress in Spinal Cord Injury: Pathological Roles, Molecular Targets, and Emerging Treatments: A Systematic Review.Molecular neurobiology · 2026Pooled it
- Effects of a Carbohydrate-Restricted Diet on β-Cell Response in Adults With Type 2 Diabetes.The Journal of clinical endocrinology and metabolism · 2025Trial
- CHAC1-linked NRF2 protein expression participates in pancreatic islet protection by dextrorphan.iScience · 2026Article
- Review
- Multimodal deep learning enhances genomic risk prediction for cardiometabolic diseases.Briefings in bioinformatics · 2026Article
- JNK and p53 cause human and mouse β cell death during excessive unfolded protein response.The Journal of clinical investigation · 2026Article
- Oxidative protein folding and CaCellular and molecular life sciences : CMLS · 2026Review
- Article
- QBP1 Peptide as a Potential Anti-Amyloidogenic Therapy for Type 2 Diabetes: An In Vitro Study.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The unfolded protein response and its activation by insulin in muscle are not altered by obesity or type 2 diabetes.Clinical science (London, England : 1979) · 2026Article
- The molecular mechanisms of incretin resistance in Type 2 Diabetes Mellitus (T2DM).Nutrition & diabetes · 2026Review
- Toll of Chronic Metabolic Acidosis at Molecular, Cellular, and Systemic Levels: A Conceptual Framework to Revisit Type 2 Diabetes (T2D) Pathophysiology.Biomedicines · 2026Review
- ERp46 mitigates lipotoxic ER stress to preserve GLUT2 expression and insulin secretion in β-cells.Biomedical reports · 2026Article
- Lipid Metabolism in Relation to Carbohydrate Metabolism.Advances in experimental medicine and biology · 2026Review
- GLP-1 receptor and Mitochondria-ER Contact Sites: an emerging mechanism of metabolic regulation.Frontiers in physiology · 2026Review
- LPS-TLR4 signaling attenuates CHOP-mediated apoptosis under endoplasmic reticulum stress conditions during porcine embryonic development.Frontiers in cell and developmental biology · 2026Article
- Therapeutic Effect of Rosolic Acid against Endothelial Dysfunction in Diabetic Wistar Rats.Current medicinal chemistry · 2026Article
- Single-cell virtual knockout network perturbation prioritizes candidate regulators of beta-cell functional failure in type 2 diabetes.Frontiers in endocrinology · 2026Article
- Article
- Organelle-specific crosstalk between calcium and redox signaling in pancreatic β-cells in physiology and type 2 diabetes.Frontiers in network physiology · 2026Review
267 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Given the functional importance of the endoplasmic reticulum (ER), an organelle that performs folding, modification, and trafficking of secretory and membrane proteins to the Golgi compartment, the maintenance of ER homeostasis in insulin-secreting β-cells is very important. When ER homeostasis is disrupted, the ER generates adaptive signaling pathways, called the unfolded protein response (UPR), to maintain homeostasis of this organelle. However, if homeostasis fails to be restored, the ER initiates death signaling pathways. New observations suggest that both chronic hyperglycemia and hyperlipidemia, known as important causative factors of type 2 diabetes (T2D), disrupt ER homeostasis to induce unresolvable UPR activation and β-cell death. This review examines how the UPR pathways, induced by high glucose and free fatty acids (FFAs), interact to disrupt ER function and cause β-cell dysfunction and death.
Indexed as
Identifiers
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.