Figure 2.

Scheme summarizing the role of TRP channels in cardiac fibrosis. In pathological conditions, different kind of stress stimulates Ca²⁺ entry in cardiac myocyte through TRP channels and other signaling pathway as RhoA dependent on reactive oxygen species (ROS) production, which lead to profibrotic gene’s expression. Profibrotic agonists and other stimuli activate cardiac fibroblast (green) leading to their proliferation and differentiation. The intracellular Ca²⁺ concentration increase through TRP channels promotes the expression of pro-fibrotic agonist (TGF-β1), α-SMA, collagen, and different isoforms of TRP channels, leading to exacerbated extracellular matrix synthesis and fibrosis.