Vascular smooth muscle cells
The MR is involved in the activation of numerous signaling pathways in
vascular smooth muscle cells (VSMCs) including extracellular
signal-regulated kinase (ERK), mitogen-activated protein kinase (MAPK),
the tyrosine kinase c-Src, c-jun N terminal kinase (JNK), epidermal
growth factor receptor (EGFR) or myosin phosphate target subunit-1
(MYPY1), leading to VSMC stress fiber formation, migration, inflammation
and oxidative stress (Mazak et al., 2004; Callera et al., 2005a, 2005b;
Miyata et al., 2008; Cai et al., 2017). Of special interest, aldosterone
mediated by MR activation increased the expression of Gal-3 in a dose-
and time-dependent manner in VSMCs (Calvier et al., 2013). Gal-3, via
its lectin activity, emerged as an essential factor allowing
aldosterone/MR-induced vascular inflammation and fibrosis in
vitro (Calvier et al., 2013). In summary, MR activation in VSMCs leads
to inflammation, oxidative stress and fibrosis.