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Mitochondria, Redox and Pancreatic β-Cells: Maturation, Function and Inflammatory Stress

This special issue belongs to the section “Health Outcomes of Antioxidants and Oxidative Stress“.

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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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

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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Antioxidants - ISSN 2076-3921