In this issue of Nature Metabolism, Li et al. reveal that disruptions in mitochondrial protein folding are an early trigger of β-cell dysfunction in type 2 diabetes and highlight that LONP1 has a key role in the maintenance of mitochondrial proteostasis. Boosting mitochondrial protein folding capacity may offer a promising strategy to protect β-cells and prevent or delay diabetes.
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Acknowledgements
This work was supported by NIH grants K08HD109636 (K.L.K), R01 DK093954 and DK127308 (C.E.M) and U01DK127786 and UC4DK104166 (C.E.M), VA Merit Award I01BX001733 (C.E.M), 2-SRA-2019-834-S-B, JDRF 2-SRA-2018-493-A-B, 3-IND-2022-1235-I-X (C.E.M), and gifts from the Sigma Beta Sorority, the Ball Brothers Foundation, the George and Frances Ball Foundation (C.E.M), March of Dimes Basil O’Connor Award (K.L.K). The authors thank E. Anderson-Baucum (Indiana University School of Medicine) for her edits.
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Kua, K.L., Evans-Molina, C. LONP1 loss causes mitochondrial mayhem in β-cells. Nat Metab 7, 1501–1502 (2025). https://doi.org/10.1038/s42255-025-01328-4
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DOI: https://doi.org/10.1038/s42255-025-01328-4