Fig. 1.Schematic diagram of the cellular RAS pathway in
neuroprotection, neuroinflammation, neurogenic hypertension and cellular
proliferation (see text). ACE1, angiotensin-converting enzyme 1; ACE2,
angiotensin-converting enzyme 2; ADAM-17, a member of the disintegrin and
metalloprotease adamalysin family; AGT, angiotensinogen; AKT, protein kinase B;
APA, aminopeptidase A; APC, adenomatosis polyposis coli; APN, aminopeptidase N;
AT1, angiotensin 1; ATII, angiotensin II; ATIII, angiotensin III; ATIV,
angiotensin IV; AngA, angiotensin A; Ang(1-7), angiotensin(1-7); Ang(1-9),
angiotensin(1-9); ATR, angiotensin II receptor 1; ATR, angiotensin II receptor
2; ATR, angiotensin II receptor 4; Cath B, cathepsin B; Cath D, cathepsin
D; Cath G, cathepsin G; DC, decarboxylase; ERK, extracellular signal-regulated
kinase; Fzd, Frizzled; LPR6, lipoprotein receptor-related protein 6; MAPK,
mitogen-activated protein kinase; MasR, Mas receptor; MrgD, Mas-related-G protein
coupled receptor; mTOR, mammalian target of rapamycin; NEP, neural endopeptidase;
NF-B, nuclear factor kappa-light-chain-enhancer of activated B-cells;
PIK3, phosphoinositide 3-kinase; PRR, (pro)renin receptor; ROS, reactive oxygen
species; TGF-, transforming growth factor-; VATPase, vacuolar
adenosine triphosphatase; Wnts, wingless-related integrations sites. The
processes leading to overall detrimental effects and the beneficial effects of
the RAS are indicated by red arrows and by green arrows, respectively.