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Contrary to our findings in OC cells that downregulation of CRAT decreased acetyl-CoA level, it has been reported that CRAT deficiency induces acetyl-CoA accumulation in muscle cells, suggesting that the function of CRAT in the maintenance of acetyl-CoA balance might be disrupted in cancer cells, which still needs further investigation
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Pathological expansion and dysfunction of EAT promote AF through paracrine and vasocrine secretion of pro-inflammatory and pro-fibrotic cytokines, release of extracellular vesicles carrying arrhythmogenic cargo, direct infiltration, and modulation of local electrophysiology and autonomic signaling, thereby creating a substrate for atrial cardiomyopathy, fibrosis, electrical remodeling, and AF initiation/persistence