索引超出了数组界限。
[1] Schulze CJ, Wang W, Kumari R, et al. Imbalance between tissue inhibitor of metalloproteinase-4 and matrix metalloproteinases during acute myocardial correction of myocardial ischemia-reperfusion injury [J]. Circulation,2003,107(19):2487-2492.
[2] 赵潇然,张凤如.心肌再灌注损伤的机制与治疗策略[J]. 国际心血管病杂志,2014,41(3):158-160.
[3] Palmgren MG, Nissen P. P-type ATPases [J]. Annu Rev Biophys, 2011,40: 243-266.
[4] Lingral JB. The physiological significance of the cardiotonic steroid/ ouabain-binding site of the Na+,K+-ATPase [J]. Annu Rev Physiol,2010,72: 395-412.
[5] Li Z, Cai T, Tian J, et al. NaKtide, a Na+/K+-ATPase-derived peptide Src inhibitor, antagonizes ouabain-activated signal transduction in cultured cells [J]. J Biol Chem,2009,284(31):21066-21076.
[6] Li Z, Zhang Z, Xie J, et al. Na+/K+-ATPase mimetic pNaKtide peptide inhibits the growth of human cancer cells [J]. J Biol Chem,2011,286(37): 32394-32403.
[7] Tian J, Cai T, Yuan Z, et al. Binding of Src to Na+, K+-ATPase forms a functional signaling complex [J]. Mol Biol Cell,2006,17(1):317-326.
[8] Sapia L, Palomeque J, Mattiazzi A, et al. Na+/K+-ATPase inhibition by ouabain induces CaMKⅡ-dependent apoptosis in adult rat cardiac myocytes [J]. J Mol Cell Cardiol,2010,49(3):459-468.
[9] Liu C, Bai Y, Chen Y, et al. Reduction of Na+/K+-ATPase potentiates marinobufagenin-induced cardiac dysfunction and myocyte apoptosis [J]. J Biol Chem,2012,287(20):16390-16398.
[10] Tian J, Xie ZJ. The Na+-K+-ATPase and calcium-signaling microdomains [J]. Physiology(Bethesda),2008,23:205-211.
[11] Aronsen JM, Skogestad J, Lewalle A, et al. Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase α2 activity [J]. J Physiol,2014 Oct 17. [Epub ahead of print]
[12] Despa S, Lingrel JB, Bers DM. Na+/K+-ATPase α2-isoform preferentially modulates Ca2+ transients and sarcoplasmic reticulum Ca2+ release in cardiac myocytes [J]. Cardiovasc Res,2012,95(4):480-486.
[13] Li PC, Yang YC, Hwang GY, et al. Inhibition of reverse-mode sodium-calcium exchanger activity and apoptosis by levosimendan in human cardiomyocyte progenitor cell-derived cardiomyocytes after anoxia and reoxygenation [J]. PLoS One,2014,9(2):e85909.
[14] Soliman D, Wang L, Hamming KS, et al. Late sodium current inhibition alone with ranolazine is sufficient to reduce ischemia-and cardiac glycoside-induced calcium overload and contractile dysfunction mediated by reverse-mode sodium/calcium exchange [J]. J Pharmacol Exp Ther,2012,343(2):325-332.
[15] Xu KY, Zhu W, Chen L, et al. Mechanistic distinction between activation and inhibition of(Na+/K+)-ATPase-mediated Ca2+ influx in cardiomyocyte [J]. Biochem Biophys Res Commun,2011,406(2):200-203.
[16] Guo HC, Guo F, Zhang LN, et al. Enhancement of Na+/K+ pump activity by chronic intermittent hypobaric hypoxia protected against reperfusion injury [J]. Am J Physiol Heart Circ Physiol,2011,300(6):H2280-H2287.
[17] Wang HG, Chu YF, Zou JG, et al. Antidigoxin antiserum prevents endogenous digitalis-like compound-mediated reperfusion injury via modulating sodium pump isoform gene expression [J].Can J Physiol Pharmacol,2010, 88(1):38-44.