ArticleClinical science (London, England : 1979)2023
Mitochondrial protein MPV17 promotes β-cell apoptosis in diabetogenesis.
Article in Clinical science (London, England : 1979), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Mitochondrial Homeostasis in Pancreatic β Cell Function: Mechanisms and Therapeutic Targets for Diabetes.Journal of diabetes · 2026Review
- Review
- Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026Review
- Plantamajoside: A potentially novel botanical agent for diabetes mellitus management.World journal of diabetes · 2025Article
- Mitochondrial DNA variants in the pathogenesis and metabolic alterations of diabetes mellitus.Molecular genetics and metabolism reports · 2025Review
- Identifying patterns differing between high-dimensional datasets with generalized contrastive PCA.PLoS computational biology · 2025Article
- Precision Prediction of Alzheimer's Disease: Integrating Mitochondrial Energy Metabolism and Immunological Insights.Journal of molecular neuroscience : MN · 2025Article
- Identification and validation of mitochondria-related genes in panvascular diseases.Frontiers in medicine · 2025Article
- Mitochondrial bioenergetics, metabolism, and beyond in pancreatic β-cells and diabetes.Frontiers in molecular biosciences · 2024Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
MPV17 is a mitochondrial inner membrane protein, and its deficiency can cause mitochondrial DNA (mtDNA) depletion, increase reactive oxygen species (ROS), and promote apoptosis in several cell types, suggesting that MPV17 plays a protective role in cells although the underlying mechanism remains unknown. To test whether MPV17 is also protective in diabetic kidney disease, we treated Mpv17-deficient mice with streptozotocin (STZ) and surprisingly found that they were resistant to diabetes. Mpv17 deficiency was also found to confer resistance to the diabetes induced by an insulin mutation (Ins2Akita), which represents a mouse model of monogenic diabetes characterized by proinsulin misfolding and β-cell failure. In both STZ and Ins2Akita models, Mpv17 mutants had significantly less severe β-cell loss and apoptosis compared with the wild-type mice. We next showed that MPV17 is expressed in β-cells of mice normally, suggesting that MPV17 acts β-cells autonomously to facilitate apoptosis. Consistently, Mpv17 knockdown improved the viability and ameliorated the apoptosis of cultured MIN6 cells treated with STZ and palmitic acid (PA), respectively, accompanied by prevention of caspase 3 activation. The proapoptotic effect of MPV17 in β-cells is in contrast with its known anti-apoptotic effect in other cell types. Thus, we have identified a novel regulator of β-cell death in diabetes development.
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