(KDACi) protect β-cells from inflammatory destruction in vitro and are promising immunomodulators
reverted diabetes in a mouse model of type 1 diabetes and counteracted inflammatory target cell damage.
doses that are safe and effective in human inflammatory diseases.
mechanism of action was compatible with transcription factor—rather than global chromatin—hyperacetylation, causing inhibition of transcription factor binding and reduction of proinflammatory gene expression in leukocytes and β-cells.
nsulin-producing β-cells, givinostat did not upregulate expression of the anti-inflammatory genes Socs1-3 or sirtuin-1 but reduced levels of IL-1β + IFN-γ–induced proinflammatory Il1a, Il1b, Tnfα, Fas, Cxcl2, and reduced cytokine-induced ERK phosphorylation
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