Initial research on CCG was mainly focused on its therapeutic effects regarding the cardiovascular system [26]; however, there is also promising evidence concerning a beneficial role in the above-discussed renal fibrosis and hyperproliferation [27,28,29], whereby a CCG-mediated sGC activation has been shown to reduce TGF-β expression as well as non-canonical TGF-β signaling via extracellular-regulated protein kinase 1/2 (ERK 1/2) [30,31]. Here, TGFB1 is linked to renal fibrosis.