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SERCA与心力衰竭的基因治疗 被引量：6

SERCA and gene Therapy for heart failure
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摘要 心力衰竭在现代医学研究中占有重要地位。在心力衰竭中收缩和舒张功能障碍的基本机制还不十分明确,但是在人和动物心力衰竭模型中细胞内钙离子流幅度的增大和/或减少被认为是其重要原因。在心肌舒张-收缩期,肌浆网Ca2+-ATP酶通过调节细胞内的游离钙离子浓度来发挥重要作用。本文简要对心肌肌浆网Ca2+-ATP酶的结构、功能、调节,以及在心力衰竭基因治疗方面的研究进展进行了综述。 Heart failure{CHF）is an important field in modem medical research. The mechanisms underlying the systolic and diastolic dysfunction in heart failure are unclear, but the prolongation and/or reduction in the amplitude of the intraceUular Ca2＋ transient observed in human and animal models of heart failure is thought to be a critical factor. In cardiac muscles, the sarcoplasmic retieulum Ca2＋ -ATPase （SERCA） plays a central role in the contraction-relaxation cycle of the muscle by regulating the intraceUular free Ca2 ＋. The review summarize structure, function and regulation of the sarcoplasmic reticulum Ca2＋ -ATPase and its research advancement in gane therapy filed for heart failure.
作者 王超 王林
机构地区 天津医科大学第二医院心脏科天津心脏病学研究所
出处 《中国心血管杂志》 2007年第1期72-75,共4页 Chinese Journal of Cardiovascular Medicine
基金 天津市自然科学基金(编号:05YFJMJC12500)
关键词 心力衰竭 肌浆网Ca2+-ATP酶 磷酸受钙蛋白 基因治疗 腺相关病毒 Heart failure Sarcoplasmic reficulum Ca2＋-ATPase Phospholamban Gene therapy Adeno-associated virus.
分类号 R541.6 [医药卫生—心血管疾病]
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参考文献16

  • 1Brixius K, Frank KF, Bolek B, et al. Reverse remodeling of the intracellular Ca^2+ -homeostasis: new concepts of pathophysiology and therapy of heart failure[J]. Wien Med Wochenschr, 2006,156:209-215.
  • 2Muller OJ, Lange M, Rattunde H, et al. Transgenic rat hearts overexpressing SERCA2a show improved contractility under baseline conditions and pressure overload[J]. Cardiovascular Research, 2003, 59:380-389.
  • 3Frank KF, Bolck B, Erdmann E, et al. Sarcoplasmic reticulum Ca^2+-ATPase modulates cardiac contraction and relaxation [ J ].Cardiovasc Res, 2003,57: 20-27.
  • 4Janczewski AM, Zahid M, Lemster BH, et al. Phospholamban gene ablation improves calcium transients but not cardiac function in a heart failure model[J]. Cardiovascular Research, 2004, 62:468-480.
  • 5Vangheluwe P, Tjwa M, Van Den Bergh A, et al. A SERCA2 pump with an increased Ca^2+ affinity can lead to severe cardiac hypertrophy, stress intolerance and reduced life span[J]. J Mol Cell Cardiol, 2006, 41:308-317.
  • 6Periasamy M, Huke S. SERCA pump level is a critical determinant of Ca^2+ homeostasis and cardiac contractility[J]. J Mol Cell Cardiol, 2001,33 : 1053-1063.
  • 7Babu GJ, Periasamy M. Transgenic mouse models for cardiac dysfunction by a specific gene manipulation [ J ]. Methods Mol Med, 2005, 112:365-377.
  • 8Weisser-Thomas J, Kubo H, Hefner CA, et al. The Na^+/Ca^2+ exchanger/SR Ca^2+ ATPase transport capacity regulates the contractility of normal and hypertrophied feline ventricular myocytes[J]. J Card Fail, 2005, 11:380-387.
  • 9Mihra S, Sabbah HN, Rastogi S, et al. Reduced sarcoplasmic reticulum Ca^2+ uptake and increased Na^+-Ca^2+ exchanger expression in left ventricle myocardium of dogs with progression of heart failure[J]. Heart Vessels, 2005, 20:23-32.
  • 10Stull LB, Matteo RG, Sweet WE, et al. Changes in calcium cycling precede cardiac dysfunction during autoimmune myocarditis in mice[J]. J Mol Cell Cardiol, 2001, 33:449-460

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中国心血管杂志
2007年 第1期

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