Using a human intestinal myofibroblast model and biopsy samples from patients with cardiovascular disease (CD)), it was shown that although increased TRPC6 (and presumably TRPC4) activity promotes the TGFbeta1-mediated expression of alpha-Smooth Muscle Actin (a-SMA) and N-cadherin and strengthens interactions between the 2 molecules, it also negatively regulates collagen synthesis and the secretion of antifibrotic factors, such as IL-10 and IL-11. Here, IL11 is linked to cardiovascular disorder.