Genetically Modified Mouse Models Used for Studying the Role of the AT2 Receptor in Cardiac Hypertrophy and Heart Failure

被引:10
|
作者
Avila, Maria D. [2 ]
Morgan, James P. [1 ]
Yan, Xinhua [1 ]
机构
[1] Tufts Univ, St Elizabeths Med Ctr, Sch Med, Dept Cardiovasc Res, Boston, MA 02135 USA
[2] Tufts Univ, Sch Med, Carney Hosp, Dept Internal Med, Boston, MA 02124 USA
关键词
II TYPE-2 RECEPTOR; TRANSGENIC MICE; MYOCARDIAL-INFARCTION; PRESSURE-OVERLOAD; ANGIOTENSIN; GROWTH; OVEREXPRESSION; FIBROBLASTS; EXPRESSION; MYOCYTES;
D O I
10.1155/2011/141039
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The actions of Angiotensin II have been implicated in many cardiovascular conditions. It is widely accepted that the cardiovascular effects of Angiotensin II are mediated by different subtypes of receptors: AT(1) and AT(2). These membrane-bound receptors share a part of their nucleic acid but seem to have different distribution and pathophysiological actions. AT(1) mediates most of the Angiotensin II actions since it is ubiquitously expressed in the cardiovascular system of the normal adult. Moreover AT(2) is highly expressed in the developing fetus but its expression in the cardiovascular system is low and declines after birth. However the expression of AT(2) appears to be modulated by pathological states such as hypertension, myocardial infarction or any pathology associated to tissue remodeling or inflammation. The specific role of this receptor is still unclear and different studies involving in vivo and in vitro experiments have shown conflicting data. It is essential to clarify the role of the AT(2) receptor in the different pathological states as it is a potential site for an effective therapeutic regimen that targets the Angiotensin II system. We will review the different genetically modified mouse models used to study the AT(2) receptor and its association with cardiac hypertrophy and heart failure.
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页数:5
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