Figure 1.

The main mechanisms of H₂S-mediated protection against fibrosis development. H₂S plays a complex role in the development of fibrosis. Besides as a reductant to directly scavenge oxygen free radicals, H₂S exerts its inhibitory effect on fibrosis by anti-inflammation, selectively anti- or proapoptosis, proangiogenic effect, and suppression of fibroblasts activation. Many signaling pathways such as NF-κB, Akt, MAPKs, TGF-β1/Smad, and HO-1 and the activity of calcium and potassium channels are involved in the process of antifibrosis of H₂S. The excitatory effects are denoted by the lines with arrow ends, and the inhibitory effects are indicated by the lines with bar ends. ROS/RNS: reactive oxygen and nitrogen species; GSH: glutathione; TNF-α: tumor necrosis factor-α; NF-κB: nuclear factor-kappa B; Akt: protein kinase B; MAPKs: mitogen-activated protein kinases; TGF-β1: transforming growth factor beta-1; Nrf2: nuclear factor E2-related factor; HO-1: heme oxygenase 1; VEGF: vascular endothelial growth factor; K_ATP: ATP-sensitive potassium channels.