运动性心肌肥大及其信号通路研究进展
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摘要
传统理论认为,运动性心肌肥大体现了机体对系统训练的生理适应,但最新的研究结果表明,运动诱导的心肌肥大会导致机体出现一些病理性的改变.相关研究证实,无论生理性心肌肥大或病理性心肌肥大,均具有鲜明的结构和分子基础,最具特征的信号通路则是PI3K和Gq信号通路.在介绍运动性心肌肥大机制的基础上,对心肌肥大的分类以及信号通路进行综述,以期更好地了解运动性心肌肥大,从而将运动性心肌肥大风险控制在最小范围.
Traditional theory holds that exercise-induced myocardial bypertrophy embodies the physiological adaptation of the body to the system training,but the recent research on the exercise-induced myocardial hypertrophy properties has generated controversy,saying that some pathological changes occur.The related research shows that the physiological myocardial hypertrophy and pathological myocardial hypertrophy have a distinct structure and molecular basis.The most typical signaling pathway is PI3K and Gq signaling pathways.In this paper,on the basis of the introduction of exercise-induced myocardial hypertrophy,the paper summarizes the classification of myocardial hypertrophy and its signaling pathways for better understanding of the exercise-induced myocardial hypertrophy,the minimization in risk control of exercise-induced myocardial hypertrophy.
Traditional theory holds that exercise-induced myocardial bypertrophy embodies the physiological adaptation of the body to the system training,but the recent research on the exercise-induced myocardial hypertrophy properties has generated controversy,saying that some pathological changes occur.The related research shows that the physiological myocardial hypertrophy and pathological myocardial hypertrophy have a distinct structure and molecular basis.The most typical signaling pathway is PI3K and Gq signaling pathways.In this paper,on the basis of the introduction of exercise-induced myocardial hypertrophy,the paper summarizes the classification of myocardial hypertrophy and its signaling pathways for better understanding of the exercise-induced myocardial hypertrophy,the minimization in risk control of exercise-induced myocardial hypertrophy.
引文
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[17]Sodha N R,Clements R T,Bianchi C,et al.Cardiopulmonary bypass with cardioplegic arrest activates protein kinase C in the human myocardium[J].J Am Coll Surg,2008,206(1):33-41.
[18]Lay A J,Northway C M,Donahue D L,et al.Low levels of tissue factor rescue protein C-associated pregnancy failure in mice[J].J Thromb Haemost,2008,6(10):1815-1817.
[19]Wang Q J.PKD at the crossroads of DAG and PKC signaling[J].Trends Pharmacol Sci,2006,27(6):317-323.
[20]李欣,徐波.中等强度耐力运动对心脏局部AngII及ATIR表达的影响[J].北京体育大学学报,2013,36(8):67-71.
[21]李欣.中等强度耐力训练对心脏Akt/mTOR信号通路表达的影响[J].北京体育大学学报,2014,37(8):77-82.
[2]Beltrami A P,Barlucchi L,Torella D,et al.Adult cardiac stem cells are multipotent and support myocardial regeneration[J].Cell,2003,114(6):763-776.
[3]Meerson F Z,Katz A M.The failing heart,adaptation and de-adaptation[M].New York,USA:Raven Press,1983.
[4]Dorn G W.The fuzzy logic of physiological cardiac hypertrophy[J].Hypertension,2007,49(5):962-970.
[5]Richey P A,Brown S P.Pathological versus physiological left ventricular hypertrophy:A review[J].J Sports Sci,1998,16(2):129-141.
[6]Pluim B M,Zwinderman A H,van der Laarse A,et al.The athlete's heart A meta-analysis of cardiac structure and function[J].Circulation,2000,101(3):336-344.
[7]Lauschke J,Maisch B.Athlete's heart or hypertrophic cardiomyopathy?[J].Clin Res Cardiol,2009,98(2):80-88.
[8]Hirsch E,Costa C,Ciraolo E.Phosphoinositide 3-kinases as a common platform for multi-hormone signaling[J].J Endocrinol,2007,194(2):243-256.
[9]Haga S,Ozaki M,Inoue H.The survival pathways phosphatidylinositol-3 kinase(PI3-K)/phosphoinositide-dependent protein kinase 1(PDK1)/Akt modulate liver regeneration through hepatocyte size rather than proliferation[J].Hepatology,2009,49(1):204-214.
[10]Foster K G,Fingar D C.Mammalian target of rapamycin(mTOR):Conducting the cellular signaling symphony[J].J Biol Chem,2010,285(19):14071-14077.
[11]D'Angelo D D,Sakata Y,Lorenz J N,et al.Transgenic Gq overexpression induces cardiac contractile failure in mice[J].Proc Natl Acad Sci U S A,1997,94(15):8121-8126.
[12]Bunney T D,Baxendale R W,Katan M.Regulatory links between PLC enzymes and ras superfamily GTPases:Signalling via PLCepsilon[J].Adv Enzyme Regul,2009,49(1):54-58.
[13]Jalili T,Takeishi Y,Walsh R A.Signal transduction during cardiac hypertrophy:The role of G alpha q,PLC beta I,and PKC[J].Cardiovasc Res,1999,44(1):5-9.
[14]Litosch I.G-protein betagamma subunits antagonize protein kinase C-dependent phosphorylation and inhibition of phospholipase C-beta1[J].Biochem J,1997,326(3):701-707.
[15]Yang C,Kazanietz M G.Divergence and complexities in DAG signaling:Looking beyond PKC[J].Trends Pharmacol Sci,2003,24(11):602-608.
[16]Kalive M,Faust J J,Koeneman B A,et al.Involvement of the PKC family in regulation of early development[J].Mol Reprod Dev,2010,77(2):95-104.
[17]Sodha N R,Clements R T,Bianchi C,et al.Cardiopulmonary bypass with cardioplegic arrest activates protein kinase C in the human myocardium[J].J Am Coll Surg,2008,206(1):33-41.
[18]Lay A J,Northway C M,Donahue D L,et al.Low levels of tissue factor rescue protein C-associated pregnancy failure in mice[J].J Thromb Haemost,2008,6(10):1815-1817.
[19]Wang Q J.PKD at the crossroads of DAG and PKC signaling[J].Trends Pharmacol Sci,2006,27(6):317-323.
[20]李欣,徐波.中等强度耐力运动对心脏局部AngII及ATIR表达的影响[J].北京体育大学学报,2013,36(8):67-71.
[21]李欣.中等强度耐力训练对心脏Akt/mTOR信号通路表达的影响[J].北京体育大学学报,2014,37(8):77-82.