ReviewExperimental diabetes research2012
Mitochondrial dysfunction and β-cell failure in type 2 diabetes mellitus.
Review in Experimental diabetes research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 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.
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Who cites it
111 citing papers in PubMed, 216 citations in OpenAlex.
- Compositional recalibrations of cardiolipin integrate loss of stearoyl-CoA desaturase 1 activity with mitochondrial decay in lipid-laden pancreatic β-cells.Cell communication and signaling : CCS · 2026Article
- Redox Imbalance in Gestational Diabetes Mellitus: Mechanistic Insights, Emerging Biomarkers, and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Integrated biophysical and spatial remodeling during insulin secretory granule maturation at the mitochondrial network.bioRxiv : the preprint server for biology · 2026Article
- Multi-Omics Analysis of a Spontaneous Type 2 Diabetes Model inInternational journal of molecular sciences · 2026Article
- Circular RNAs as diagnostic biomarkers in type 2 diabetes mellitus: implications in metabolic dysfunction and immune-inflammatory crosstalk.Frontiers in immunology · 2026Review
- Identification of mitochondria-related key genes in type 2 diabetes mellitus and elucidation of the Zhimu-Huangbai herb Pair's mechanism: an integrated approach of bioinformatics, machine learning, and experimental validation.Frontiers in cell and developmental biology · 2026Article
- NMR-Based Serum Metabolomics and Correlation Analysis Unraveled Metabolic Alterations Underlying Pathophysiology of Type 2 Diabetes Mellitus.ACS omega · 2025Article
- LONP1 regulation of mitochondrial protein folding provides insight into beta cell failure in type 2 diabetes.Nature metabolism · 2025Article
- Hepatic and Pancreatic Cellular Response to Early Life Nutritional Mismatch.Endocrinology · 2025Article
- Adrenic acid: A promising biomarker and therapeutic target (Review).International journal of molecular medicine · 2025Review
- Systems Pharmacology-based Drug Discovery and Active Mechanism ofCurrent pharmaceutical design · 2025Article
- Mitochondrial uncoupling protein 2: a central player in pancreatic disease pathophysiology.Molecular medicine (Cambridge, Mass.) · 2024Review
- Role of cytosolic and endoplasmic reticulum CaPflugers Archiv : European journal of physiology · 2024Review
- SORCS2 activity in pancreatic α-cells safeguards insulin granule formation and release from glucose-stressed β-cells.iScience · 2024Article
- Complex II ambiguities-FADHThe Journal of biological chemistry · 2024Review
- CaFrontiers in endocrinology · 2024Review
- Mitochondrial Dysfunction and Imeglimin: A New Ray of Hope for the Treatment of Type-2 Diabetes Mellitus.Mini reviews in medicinal chemistry · 2024Review
- Identification of reversible and druggable pathways to improve beta-cell function and survival in Type 2 diabetes.Islets · 2023Article
- Antioxidant and Antidiabetic Properties of a Thinned-Nectarine-Based Nanoformulation in a Pancreatic β-Cell Line.Antioxidants (Basel, Switzerland) · 2023Article
- Glucose-Lowering Effects of Imeglimin and Its Possible Beneficial Effects on Diabetic Complications.Biology · 2023Review
51 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Type 2 diabetes mellitus (T2DM) is the most common human endocrine disease and is characterized by peripheral insulin resistance and pancreatic islet β-cell failure. Accumulating evidence indicates that mitochondrial dysfunction is a central contributor to β-cell failure in the evolution of T2DM. As reviewed elsewhere, reactive oxygen species (ROS) produced by β-cell mitochondria as a result of metabolic stress activate several stress-response pathways. This paper focuses on mechanisms whereby ROS affect mitochondrial structure and function and lead to β-cell failure. ROS activate UCP2, which results in proton leak across the mitochondrial inner membrane, and this leads to reduced β-cell ATP synthesis and content, which is a critical parameter in regulating glucose-stimulated insulin secretion. In addition, ROS oxidize polyunsaturated fatty acids in mitochondrial cardiolipin and other phospholipids, and this impairs membrane integrity and leads to cytochrome c release into cytosol and apoptosis. Group VIA phospholipase A₂ (iPLA₂β) appears to be a component of a mechanism for repairing mitochondrial phospholipids that contain oxidized fatty acid substituents, and genetic or acquired iPLA₂β-deficiency increases β-cell mitochondrial susceptibility to injury from ROS and predisposes to developing T2DM. Interventions that attenuate ROS effects on β-cell mitochondrial phospholipids might prevent or retard development of T2DM.
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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.