【摘要】：心力衰竭在細(xì)胞水平主要表現(xiàn)為心肌以興奮-收縮耦聯(lián)(excitement-contraction coupling,ECC)為基礎(chǔ)的收縮功能障礙,而Ca2+信號轉(zhuǎn)導(dǎo)在此過程中起著非常重要的作用。肌漿網(wǎng)(sarcoplasmic reticulum,SR)蘭尼堿受體(ryanodine receptor type 2,RyR2)是心肌最重要的鈣釋放通道,RyR2磷酸化是肌漿網(wǎng)鈣釋放的基礎(chǔ),而RyR2磷酸化主要受蛋白激酶A(protein kinase A,PKA)和鈣離子/鈣調(diào)蛋白依賴性蛋白激酶Ⅱ(calcium/calmodulin dependent protein kinaseⅡ,CaMKⅡ)的調(diào)控。目前對RyR2磷酸化的研究已經(jīng)非常廣泛,但對其涉及心力衰竭的具體發(fā)病機(jī)制仍有爭議,本綜述主要針此問題進(jìn)行闡述。
[Abstract]:Heart failure is characterized by contraction dysfunction based on excitation-contraction coupling (excitement-contraction coupling,ECC) at cellular level, and Ca2 signal transduction plays a very important role in this process. Sarcoplasmic reticulum (sarcoplasmic reticulum,SR) (ryanodine receptor type _ 2 (ryanodine receptor type _ 2 RyR2 is the most important calcium release channel in myocardium. RyR2 phosphorylation is the basis of sarcoplasmic reticulum calcium release, while RyR2 phosphorylation is mainly caused by protein kinase A (protein kinase A,. PKA and calcium/calmodulin dependent protein kinase 鈪，

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