Substantial experimental evidences support the hypothesis that dietary flavonoid intake has a favourable impact on cardiovascular diseases such as systemic, arterial hypertension and coronary artery diseases, which represent the leading cause of morbidity and mortality worldwide. The biological effects of flavonoids involve complex biochemical interactions with numerous, specific, cellular and molecular targets. K+ channels, fine modulators of both cardiac action potential and vascular cell membrane potential, represent one of these targets. Overexpression, downregulation or dysfunction of these channel proteins are the cause of many cardiovascular diseases. Therefore, it appears of particular interest a detailed analysis of the flavonoid potential, direct/indirect modulation of cardiovascular K+ channels as these natural compounds ingested with the diet, despite extensive gut metabolism, may accumulate at cellular level in the form of the parent aglycones. The present review will portray their effects on cardiovascular K+ channels. Molecular docking was used to strengthen experimental evidences and describe flavonoid-channel interactions at molecular level.
Keywords: Acacetin (PubChem CID: 5280442); Apigenin (PubChem CID: 5280443); Apigenin trimethyl-ether (PubChem CID: 79730); Daidzein (PubChem CID: 5281708); Docking simulation; Epicatechin (PubChem CID: 72276); Epicatechin gallate (PubChem CID: 107905); Epigallocatechin (PubChem CID: 72277); Epigallocatechin gallate (PubChem CID: 65064); Flavonoid; Genistein (PubChem CID: 5280961); Hesperetin (PubChem CID: 72281); Kaempferol (PubChem CID: 5280863); Morin (PubChem CID: 5281670); Myricetin (PubChem CID: 5281672); Naringenin (PubChem CID: 932); Naringin (PubChem CID: 442428); Patch-clamp; Potassium channel; Puerarin (PubChem CID: 5281807); Quercetin (PubChem CID: 5280343).
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