Figure 1.

This figure illustrates the various molecular and signaling paradigms through which H₂S contributes to vasodilation: 1. Persulfidation Signaling—a post-translational modification where a sulfur atom is added to the thiol (-SH) group of cysteine residues, forming persulfide (-SSH) groups; 2. K_ATP Channel Activation Paradigm—reduces calcium influx, resulting in smooth muscle relaxation and vasodilation; 3. cGMP Pathway Activation Paradigm—elevated cGMP activates protein kinase G (PKG), which decreases intracellular calcium levels, causing smooth muscle relaxation and vasodilation; 4. Endothelial Nitric Oxide Synthase (eNOS) activation Paradigm; 5. Calcium Signaling Modulation Paradigm; 6. Redox Signaling and Antioxidant Effects Paradigm; 7. Interaction with Other Gasotransmitters Paradigm; 8. Endothelial-Dependent Hyperpolarization (EDH) Paradigm; 9. Interaction with Prostacyclin Signaling Paradigm; 10. Hypoxia Response Paradigm; 11. H₂S interaction with various transcription factors.