ReviewCells2025
β-Cell Mitochondrial Dysfunction: Underlying Mechanisms and Potential Therapeutic Strategies.
Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed.
- Mitochondrial structural and functional aberrations in diabetic bladder dysfunction: underlying mechanisms and therapeutic landscapes.Acta diabetologica · 2026Review
- Hair-Based Biomonitoring of Phthalate Metabolites and Triclosan in Childhood: Links with Metabolic and Endocrine Disorders.Journal of xenobiotics · 2026Article
- Oxidative Stress Biomarkers in Pediatric and Early-Stage Type 1 Diabetes: Toward Redox Phenotyping.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondrial Quality Control in Age-Related Diseases: From Molecular Architecture to Precision Therapeutics.Antioxidants (Basel, Switzerland) · 2026Review
- MitoQ Triggers Mitochondrial Collapse and Apoptotic Death in Glioblastoma Associated with KATP Channel Expression Changes.Neurochemical research · 2026Article
- Age-Specific Association Between Urinary Phthalate Metabolites and Diabetes Mellitus: Findings from the Korean National Environmental Health Survey Cycle 4 (2018-2020).Healthcare (Basel, Switzerland) · 2026Article
- Article
- Stress-driven remodeling of antigen presentation and chemokine signaling in pancreatic β-cells: implications for type 1 diabetes.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are essential for β-cell function, coupling glucose metabolism to ATP production and insulin secretion. In diabetes, β-cell mitochondrial dysfunction arises from oxidative stress, impaired quality control and disrupted dynamics, leading to reduced oxidative phosphorylation, defective insulin release and progressive cell loss. Key transcriptional regulators link genetic susceptibility to mitochondrial dysfunction in both type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). These disruptions impair mitophagy, mitochondrial translation and redox homeostasis. Therapeutic strategies that restore mitochondrial function, including mitophagy enhancers, mitochondrial antioxidants, and transcriptional regulators, have shown potential in preserving β-cell integrity. As mitochondrial failure precedes β-cell loss, targeting mitochondrial pathways may represent a critical approach to modifying diabetes progression.
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What OpenQuestion holds
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.