HL-1心房筋細胞におけるAkt-HSF1-Hsp70経路を介したKv1.5蛋白質発現およびチャネル活性の尿酸誘発性増強

increase the protein level of voltage-gated potassium channel subfamily 1 number 5 (Kv1.5)by increasing the NADPHdependent oxidative stress level in HL-1 mouse atrial myocytes.8 Uric acid may lead to inductions of arrhythmias including AF and resultant increases in cardiovascular mortality via the enhancement of Kv1.5 expression.However, precise molecular mechanisms underlying the uric U ric acid is the end product of purine catabolism in a human body. 1 Many reports indicated a positive correlation between serum uric acid concentration and morbidity or mortality of cardiovascular diseases including atrial fibrillation (AF).2-5 It is well known that increases in potassium channel currents shorten the atrial refractory period to facilitate the development of re-entry circuits, leading to AF. Escalation of cardiovascular morbidity and mortality has been attributed to oxidative stress.6,7 Our previous study indicated that uric acid could