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Experimental findings in mouse KD models demonstrate that reduced abundance of specific Clostridium (e.g., Clostridium sensu stricto , Clostridium clusters XIVa ) correlates significantly with vasculitis progression, whereas supplementation with these Clostridium or SCFAs alleviates vascular inflammation by either activating G protein-coupled receptors (GPR43/109A) or inhibiting HDAC activity

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Its defining feature is CD36 receptor interaction in cardiac tissue, producing cardioprotection independent of GH release, demonstrated definitively in CD36 knockout mouse models