Full text is available at the source.
Abstract
Mitochondrial dysfunction is linked to compromised β-cell survival and insulin secretion in Type 1 Diabetes (T1D).
- Autoimmune inflammation disrupts mitochondrial balance, leading to oxidative stress and impaired calcium signaling.
- Dysregulation of mitochondrial quality control mechanisms, such as fusion-fission dynamics and mitophagy, contributes to β-cell dysfunction.
- Mitochondrial proteins like olfactomedin-4 may modulate insulin release and serve as potential therapeutic targets.
- Crosstalk between the endoplasmic reticulum and mitochondria plays a role in β-cell apoptosis, particularly via CHOP signaling.
- Pharmacological interventions have demonstrated effectiveness in preserving mitochondrial function and enhancing β-cell activity in animal studies.
Simplified