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Title:: -

作者:: 侯江龙; 马建旸; 四川大学华西医院胸心血管外科，四川成都 610041

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关键词:: 心肌细胞; 再生; 细胞周期

Keywords:: -

分类号:: R654.2

DOI:: -

文献标识码:: A

摘要:: 传统认为，哺乳动物心脏细胞在出生后不久即失去了有丝分裂的能力，成为终末分化的有丝分裂后的细胞。然而，近年研究表明，人类心脏完全有可能在损伤一段时间后，通过心肌细胞分裂和再生进行自然的修复。对心肌细胞在蛋白分子和基因水平上进行调节，可重新激活和提高心肌细胞分裂和增殖的潜能，以替代坏死及纤维化的心肌细胞，有望成为缺血性心脏病、心力衰竭等患者促进心脏自我修复，改善心脏功能的新的治疗方向。现将近年来对成熟心肌细胞周期进行调控，从而诱导其重新进入有丝分裂的研究进展进行了综述。

Abstract:: -

参考文献/References

［1］王月刚，吴平生. 干细胞移植治疗冠心病的应用进展［J］. 心脏杂志, 2007, 19(1)：91-95.

［2］Ahuja P, Sdek P, MacLellan WR. Cardiac myocyte cell cycle control in development, disease, and regeneration［J］. Physiol Rev, 2007, 87(2):521-544.

［3］Bicknell KA, Coxon CH, Brooks G. Can the cardiomyocyte cell cycle be reprogrammed?［J］. J Mol Cell Cardiol, 2007, 42(4):706-721.

［4］Tousoulis D, Briasoulis A, Antoniades C, et al. Heart regeneration: what cells to use and how?［J］. Curr Opin Pharmacol, 2008, 8(2):211-218.

［5］Bicknell KA, Brooks G. Reprogramming the cell cycle machinery to treat cardiovascular disease［J］. Curr Opin Pharmacol, 2008, 8(2):193-201.

［6］Cheng RK, Asai T, Tang H, et al. Cyclin A2 induces cardiac regeneration after myocardial infarction and prevents heart failure［J］. Circ Res, 2007, 100(12):1741-1748.

［7］Evans-Anderson HJ, Alfieri CM, Yutzey KE. Regulation of cardiomyocyte proliferation and myocardial growth during development by FOXO transcription factors［J］. Circ Res, 2008, 102(6):686-694.br />
［8］Zhong W, Mao S, Tobis S, et al. Hypertrophic growth in cardiac myocytes is mediated by Myc through a Cyclin D2-dependent pathway［J］. EMBO J, 2006, 25(16):3869-3879.

［9］Cheng RK, Asai T, Tang H, et al. Cyclin A2 induces cardiac regeneration after myocardial infarction and prevents heart failure［J］. Circ Res, 2007, 100(12):1741-1748.

［10］Williams SD, Zhu H, Zhang L, et al. Adenoviral delivery of human CDC5 promotes G2/M progression and cell division in neonatal ventricular cardiomyocytes［J］. Gene Ther, 2006, 13(10):837-843.

［11］Zhai P, Gao S, Holle E, et al. Glycogen synthase kinase-3alpha reduces cardiac growth and pressure overload-induced cardiac hypertrophy by inhibition of extracellular signal-regulated kinases［J］. J Biol Chem, 2007, 282(45):33181-33191.

［12］Hirotani S, Zhai P, Tomita H, et al. Inhibition of glycogen synthase kinase 3beta during heart failure is protective［J］. Circ Res, 2007, 101(11):1164-1174.

［13］Tseng AS, Engel FB, Keating MT. The GSK-3 inhibitor BIO promotes proliferation in mammalian cardiomyocytes［J］. Chem Biol, 2006, 13(9):957-963.

［14］Wang Y. Mitogen-activated protein kinases in heart development and diseases［J］. Circulation, 2007, 116(12):1413-1423.

［15］Kompa AR, See F, Lewis DA, et al. Long-term but not short-term p38 mitogen-activated protein kinase inhibition improves cardiac function and reduces cardiac remodeling post-myocardial infarction［J］. J Pharmacol Exp Ther, 2008, 325(3):741-750.

［16］Engel FB, Hsieh PC, Lee RT, et al. FGF1/p38 MAP kinase inhibitor therapy induces cardiomyocyte mitosis, reduces scarring, and rescues function after myocardial infarction［J］. Proc Natl Acad Sci USA, 2006, 103(42):15546-15551.

［17］Norris RA, Borg TK, Butcher JT, et al. Neonatal and adult cardiovascular pathophysiological remodeling and repair: developmental role of periostin［J］. Ann N Y Acad Sci, 2008, 1123:30-40.

［18］Shimazaki M, Nakamura K, Kii I, et al. Periostin is essential for cardiac healing after acute myocardial infarction［J］. J Exp Med, 2008, 205(2):295-303.

［19］Dorn GW 2nd. Periostin and myocardial repair, regeneration, and recovery［J］. N Engl J Med, 2007, 357(15):1552-1554.

［20］Kühn B, del Monte F, Hajjar RJ, et al. Periostin induces proliferation of differentiated cardiomyocytes and promotes cardiac repair［J］. Nat Med, 2007, 13(8):962-969.

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心肌细胞周期调控方法的研究进展

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

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