Michael S, Marber, Beth Rose, et al. The p38 Mitogen-activated protein kinases pathway―A potential target for intervention in infarction, hypertrophy, and heart failure[J]. Journal of Molecular and cellular cardiology, 2011,51:485-90
[6]
Kanda T, Takahashi T. Interleukin-6 and cardiovascular diseases[J].Jpn Heart J,2004,45:183？193.
[7]
Kubota T, McTiernan CF, Frye CS, et al. Dilated cardiomyopathy in transgenic mice with cardiac-specific overexpression of tumor necrosis factor-alpha[J]. Circ Res, 1997, 81:627？635.
[8]
Bryant D, Becker L, Richardson J, et al. Cardiac failure in transgenic mice with myocardial expression of tumor necrosis factor-α[J]. Circulation,1998, 97: 1340-1341.
[9]
Kubota T, Miyagishima M, Alvarez RJ, et al. Expression of proinflammatory cytokines in the failing human heart: comparison of recent-onset and end-stage congestive heart failure[J]. J Heart Lung Transplant, 2000, 19:819？824.
[10]
Li M, Georgakopoulos D, Lu G, et al. p38 MAP Kinase Mediates Inflammatory Cytokine Induction in Cardiomyocytes and Extracellular Matrix Remodeling in Heart[J].Circulation,2005,111:2494-2502.
[11]
Sicard P, Clark JE, Jacquet S, et al.The activation of p38 alpha, and not p38beta, mitogen-activated protein kinase is required for ischemic preconditioning[J]. J Mol Cell Cardiol,2010,48:1324-328.
[12]
Nishida K, Yamaguchi O, Hirotani S, et al. P38 alpha mitogen-activated protein kinase plays a critical role in cardiomyocyte survival but not in cardiac hypertrophic growth in response to pressure overload[J]. Mol Cell Biol,2004,24:10611-10620.
