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Summary Pancreatic β-cell failure in diabetes is driven by chronic inflammation, yet how metabolic stress determines pro-inflammatory cell fate remains unclear. Here, we report that sublethal oxidative stress activates a β-cell-enriched epigenetic switch that licenses intrinsic inflammation. We identify a β-cell-enriched vulnerability wherein oxidative stress disrupts mitochondrial NAD⁺/acetyl-CoA flux, skewing the nuclear equilibrium between the deacetylase SIRT1 and acetyltransferases p300/CBP.
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
