Mitochondria, Redox and Pancreatic β-Cells: Maturation, Function and Inflammatory Stress
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: 30 November 2026 | Viewed by 2074
Special Issue Editor
Special Issue Information
Dear Colleagues,
Type 2 diabetes is a common condition whereby pancreatic β-cells fail to match insulin secretion to metabolic demand, especially under nutrient overload and maladaptation. This Special Issue focuses on the mitochondrial–redox axis that underpins β-cell identity, stimulus–secretion coupling, and stress vulnerability. We welcome basic, translational, and clinical studies clarifying how mitochondrial bioenergetics, dynamics, and quality control intersect with redox signaling to shape β-cell maturation, insulin secretory competence, and resilience—or susceptibility—to cytokines, lipotoxicity, glucotoxicity, and islet inflammation. Topics include respiratory-chain control of ATP/ADP coupling; ER–mitochondria Ca2+ crosstalk; ROS/RNS signaling and antioxidant defenses; mitochondrial dynamics, biogenesis, UPR^mt, and mitophagy; metabolic inflexibility, dedifferentiation, and senescence; innate immune pathways and inflammasome activation; extracellular vesicles and redox communication; single-cell multi-omics; advanced imaging; human islets and iPSC-derived organoids; biomarkers of mitochondrial/redox dysfunction; and mitochondria- or redox-targeted therapeutics. Our goal is to present a forward-looking collection of studies that advance our understanding of the mechanisms of β-cell function and yield testable diagnostics and therapies for its preservation. Topics of interest include the following:
- Mitochondrial bioenergetics, ETC dysfunction, and insulin secretion;
- Redox signaling, oxidative stress, and antioxidant defenses in β-cells;
- Mitophagy, UPR^mt, and mitochondrial quality control under inflammatory stress;
- ER–mitochondria Ca2+ crosstalk and metabolic coupling;
- β-cell maturation, identity, dedifferentiation, and senescence in T1D/T2D contexts;
- Cytokine signaling, inflammasomes, and islet immune–metabolic interfaces;
- Extracellular vesicles and redox-mediated intercellular communication;
- Human islets, iPSC-derived β-cells, organoids;
- Single-cell/spatial omics and imaging;
- Biomarkers and noninvasive readouts of mitochondrial/redox status;
- Therapeutic strategies.
Dr. Sarah Zangen
Guest Editor
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Keywords
- pancreatic β-cell mitochondria
- redox
- ETC dysfunction
- electron ROS/RNS
- mitophagy
- UPR^mt
- antioxidant defenses
- cytokines
- inflammasome
- iPSC/islet organoids
- biomarkers
- therapeutics
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