ArticleNature communications2025
UCP2 inhibition eliminates pancreatic β cell autoinflammation in T2DM with islet-mitochondrial sequential targeting nanomedicines.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed.
- Glycemic status-dependent proteomic signatures of biological aging for health risk prediction.GeroScience · 2026Article
- cGAS-STING signaling in aging and age-related diseases: therapeutic promise and precaution.Archives of pharmacal research · 2026Review
- Mitochondrial Homeostasis in Pancreatic β Cell Function: Mechanisms and Therapeutic Targets for Diabetes.Journal of diabetes · 2026Review
- Natural Product Rengyolone Attenuates LPS-Induced Microglia Inflammation via Suppression of the TLR4/NF-κB Pathway.Chemistry & biodiversity · 2026Article
- Review
- Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026Review
- Vitamin D alleviates type 2 diabetes by promoting autophagy and inhibiting inflammation via the NLRP3 inflammasome pathway.Open life sciences · 2026Article
- Mito-Genipin, a Novel Mitochondria-Targeted Genipin Derivative Modulates Oxidative Stress and Inflammation in Macrophages.Antioxidants (Basel, Switzerland) · 2025Article
- Pharmacological and non-pharmacological modulation of endoplasmic reticulum stress in pediatric diabetes.Frontiers in endocrinology · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Pancreatic β-cell dysfunction and mass loss are core pathologies of type 2 diabetes mellitus (T2DM), which are closely related to intense autoinflammation. However, the molecular mechanisms regulating β-cell autoinflammation remain unclear. Here, we show that STING is significantly elevated in T2DM β cells. We also clarify the key role of uncoupling protein 2 (UCP2), and reveal that interleukin-1β (IL-1β) drives β cells to produce autoinflammation through the UCP2/mtDNA/STING axis in T2DM. To inhibit UCP2 activity in vivo, we design a tailored nanomedicine, Mito-G, with sequential targeting from islets to β-cell mitochondria. Mito-G is a negatively charged ultra-small nanomedicine synthesized by polymerization of genipin (a potent UCP2 inhibitor) and glycine. It can specifically reach β cells and have a natural mitochondrial targeting. In this work, Mito-G effectively eliminates β-cell auto-inflammation by specifically inhibiting β-cell UCP2 activity in vivo, providing a paradigm for targeting autoinflammation of β cells to treat T2DM.
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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.