Cardiomyocyte MR overexpression
Overexpression of MR in the heart resulted in dilated cardiomyopathy (Le
Menuet et al., 2001). Mice overexpressing cardiac MR did not show
increased cardiac fibrosis, inflammation or apoptosis (Latouche et al.,
2012). However, cardiac specific MR overexpression in mice induced an
increase in sudden cardiac death (Ouvrard-Pascaud et al., 2005). Mice
overexpressing MR in cardiomyocytes present increased levels of the
pro-fibrotic factor connective tissue growth factor (CTGF) (Messaoudi et
al., 2013) as well as of NGAL (Latouche et al., 2012). As mentioned
above, NGAL is a critical mediator of the pro-fibrotic and
pro-inflammatory effects of aldosterone/MR activation (Tarjus et al.,
2015; Martínez-Martínez et al., 2017a). Interestingly, NGAL inactivation
protected mice against adverse myocardial remodeling after MI
(Martínez-Martínez et al., 2017a).