Gender modulates cardiac phenotype development in genetically modified mice

被引:83
作者
Du, XJ [1 ]
机构
[1] Wynn Domain Baker Heart Res Inst, Expt Cardiol Lab, Melbourne, Vic 3004, Australia
基金
英国医学研究理事会;
关键词
hypertrophy; heart failure; gender; estrogens; transgenic animal models;
D O I
10.1016/j.cardiores.2004.03.027
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Recent research using genetically modified mice has revealed significant sex differences in cardiac phenotypes. In the majority of strains, females display a lower mortality, less severe hypertrophy, better preserved function and mitigated cardiac pathology compared with male counterparts. Thus, gender is an independent determinant for the development of cardiac phenotype in murine models. While there is strong evidence for estrogen as a cardiac protector, emerging evidence indicates adverse actions of testicular hormones that might be responsible in part for the sex differences. Studies using mouse models have also revealed novel information on signalling mechanisms mediating the sex difference. (C) 2004 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:510 / 519
页数:10
相关论文
共 83 条
[81]   Myocardial ischemia-reperfusion injury in estrogen receptor-α knockout and wild-type mice [J].
Zhai, PY ;
Eurell, RE ;
Cooke, PS ;
Lubahn, DB ;
Gross, DR .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2000, 278 (05) :H1640-H1647
[82]   Class II histone deacetylases act as signal-responsive repressors of cardiac hypertrophy [J].
Zhang, CL ;
McKinsey, TA ;
Chang, SR ;
Antos, CL ;
Hill, JA ;
Olson, EN .
CELL, 2002, 110 (04) :479-488
[83]   Abnormal vascular function and hypertension in mice deficient in estrogen receptor β [J].
Zhu, Y ;
Bian, Z ;
Lu, P ;
Karas, RH ;
Bao, L ;
Cox, D ;
Hodgin, J ;
Shaul, PW ;
Thorén, P ;
Smithies, O ;
Gustafsson, JÅ ;
Mendelsohn, ME .
SCIENCE, 2002, 295 (5554) :505-508