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.