ArticleInternational journal of molecular sciences2024
β-Cell Deletion of Hypoxia-Inducible Factor 1α (HIF-1α) Increases Pancreatic β-Cell Susceptibility to Streptozotocin.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The role of peripheral blood HIF-1α in pancreatic β-cell dysfunction and insulin resistance among patients with type 2 diabetes: a systematic review and meta-analysis.Frontiers in nutrition · 2026Pooled it
- The role of HIF-1α in innate immune mechanisms and autoimmunity: A double-edged sword.The Journal of biological chemistry · 2026Review
- Review
- Interplay of hypoxia, immune dysregulation, and metabolic stress in pathophysiology of type 1 diabetes.Frontiers in immunology · 2025Review
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Authors and funding
3 authors.
Funding
Abstract
Type 1 diabetes (T1D) is caused by the immune-mediated loss of pancreatic β-cells. Hypoxia-inducible factor 1α (HIF-1α) is a transcription factor which is crucial for cellular responses to low oxygen. Here, we investigate the role of β-cell HIF-1α in β-cell death and diabetes after exposure to multiple low-dose streptozotocin (MLDS). MDLS triggers auto-immunity in susceptible animal models, such as non-obese diabetic (NOD) mice. These experiments used a novel mouse model with β-cell-specific deletion of HIF-1α on a NOD background (BIN mice). Mice were given 20 mg/kg MLDS for 5 consecutive days. Following MLDS, 100% of BIN mice developed frank diabetes versus 33% of floxed-control (FC) littermates and 17% of NOD controls (
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Registered trials
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