ReviewFrontiers in molecular biosciences2024
Mitochondrial bioenergetics, metabolism, and beyond in pancreatic β-cells and diabetes.
Review in Frontiers in molecular biosciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- GPR180 deficiency impairs mitochondrial function and insulin secretion in pancreatic β-cells.Molecular metabolism · 2026Article
- Sirtuins as Molecular Mediators of Caloric Restriction in the Pancreas: Implications for β-Cell Function, Metabolism, and Longevity.International journal of molecular sciences · 2026Review
- Mitochondria-Targeting Metal Complexes: Design Principles, Mechanisms of Action, and Translational Perspectives.Biomolecules · 2026Review
- Addressing bioenergetic deficits and restoring mitochondrial health in transplanted islets using mesenchymal stem cells.Stem cells translational medicine · 2026Article
- Mitochondrial dysfunction-driven inflammation and β-Cell apoptosis in type 2 diabetes mellitus: mechanistic insights and therapeutic implications.Molecular biology reports · 2026Review
- Development and characterization of experimental β-cell senescence models revealing autophagy defects and altered stimulus-secretion coupling.GeroScience · 2026Article
- Multi-Omics Analysis of a Spontaneous Type 2 Diabetes Model inInternational journal of molecular sciences · 2026Article
- Stress-driven remodeling of antigen presentation and chemokine signaling in pancreatic β-cells: implications for type 1 diabetes.Frontiers in immunology · 2026Review
- Mitochondrial Dysfunction in Type 2 Diabetes and Metabolic Syndrome: Mechanisms, Biomarkers, and Emerging Therapies.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Mitochondrial development and remodeling occur at pancreatic progenitor stage during induction of stem cell-derived islet organoids.Frontiers in endocrinology · 2026Article
- GLP-1R associates with VAPB and SPHKAP at ERMCSs to regulate β-cell mitochondrial remodelling and function.Nature communications · 2025Article
- β-Cell Mitochondrial Dysfunction: Underlying Mechanisms and Potential Therapeutic Strategies.Cells · 2025Review
- Interactions between lipid droplets and mitochondria in metabolic diseases.Lipids in health and disease · 2025Review
- Molecular and Inflammatory Etiologies of β-Cell Dysfunction in Type 1 Diabetes.Physiology (Bethesda, Md.) · 2025Review
- GLP-1 receptor agonist protects glucose-stimulated insulin secretion in pancreatic β-cells against lipotoxicity via PPARδ/UCP2 pathway.Cellular and molecular life sciences : CMLS · 2025Article
- TRAF6 integrates innate immune signals to regulate glucose homeostasis via Parkin-dependent and Parkin-independent mitophagy.Science advances · 2025Article
- Leonurine (SCM-198) exerts protective effects on pancreatic β-cells in type 1 diabetes by modulating the Bax/Bcl-2/Caspase-3 signaling pathway.BMC complementary medicine and therapies · 2025Article
- Bioactive Compounds as Modulators of N-Formyl Peptide Signaling in Chronic Diseases.Molecules (Basel, Switzerland) · 2025Review
- Mitochondrial Dysfunction in Diabetes: Shedding Light on a Widespread Oversight.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- The role of mitochondrial function in the pathogenesis of diabetes.Frontiers in endocrinology · 2025Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In Type 1 and Type 2 diabetes, pancreatic β-cell survival and function are impaired. Additional etiologies of diabetes include dysfunction in insulin-sensing hepatic, muscle, and adipose tissues as well as immune cells. An important determinant of metabolic health across these various tissues is mitochondria function and structure. This review focuses on the role of mitochondria in diabetes pathogenesis, with a specific emphasis on pancreatic β-cells. These dynamic organelles are obligate for β-cell survival, function, replication, insulin production, and control over insulin release. Therefore, it is not surprising that mitochondria are severely defective in diabetic contexts. Mitochondrial dysfunction poses challenges to assess in cause-effect studies, prompting us to assemble and deliberate the evidence for mitochondria dysfunction as a cause or consequence of diabetes. Understanding the precise molecular mechanisms underlying mitochondrial dysfunction in diabetes and identifying therapeutic strategies to restore mitochondrial homeostasis and enhance β-cell function are active and expanding areas of research. In summary, this review examines the multidimensional role of mitochondria in diabetes, focusing on pancreatic β-cells and highlighting the significance of mitochondrial metabolism, bioenergetics, calcium, dynamics, and mitophagy in the pathophysiology of diabetes. We describe the effects of diabetes-related gluco/lipotoxic, oxidative and inflammation stress on β-cell mitochondria, as well as the role played by mitochondria on the pathologic outcomes of these stress paradigms. By examining these aspects, we provide updated insights and highlight areas where further research is required for a deeper molecular understanding of the role of mitochondria in β-cells and diabetes.
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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.