Genetically Modified Mouse Models Used for Studying the Role of the AT2Receptor in Cardiac Hypertrophy and Heart Failure

Author:

Avila Maria D.1,Morgan James P.2,Yan Xinhua2ORCID

Affiliation:

1. Department of Internal Medicine, Carney Hospital, Tufts University School of Medicine, Boston, MA 02124, USA

2. Department of Cardiovascular Research, St. Elizabeth's Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA

Abstract

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: AT1and AT2. These membrane-bound receptors share a part of their nucleic acid but seem to have different distribution and pathophysiological actions. AT1mediates most of the Angiotensin II actions since it is ubiquitously expressed in the cardiovascular system of the normal adult. Moreover AT2is highly expressed in the developing fetus but its expression in the cardiovascular system is low and declines after birth. However the expression of AT2appears 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 involvingin vivo and in vitroexperiments have shown conflicting data. It is essential to clarify the role of the AT2receptor 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 AT2receptor and its association with cardiac hypertrophy and heart failure.

Funder

American Heart Association

Publisher

Hindawi Limited

Subject

Health, Toxicology and Mutagenesis,Genetics,Molecular Biology,Molecular Medicine,General Medicine,Biotechnology

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