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91 Uric acid and ROS activated several proinflammatory pathways, including COX-2, suggesting that alcohol-mediated generation of these byproducts increased pulmonary inflammation, in part, via COX-2 signaling

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Conversely, disrupting this LLPS, for instance by using 1,6-hexanediol (a well-established phase separation inhibitor [45]), enhance the sensitivity of cells to heat stimulation, thereby triggering a series of endogenous apoptotic cascade signals, including Bax/Bak-related mitochondrial outer membrane permeabilization, cytochrome c release, apoptosome formation, and Caspase activation [46] (Fig