TABLE 2.
Involvement of gasotransmitters and calcium transport systems in wound healing.
| Wound healing | Acute wounds | Chronic wounds |
|---|---|---|
| Inflammation | CO-antiinflammatory effect | H2S—attenuates inflammation |
| NO- antimictobial effect | NO—suppresses inflammation, ROS scavenging | |
| H2S- antimicrobial effect | ||
| Ca2+ through TRPV—improves inflammatory wound healing | ||
| Proliferation differentiation | CO-increases proliferation, differentiation | Ca2+ blocking by azelnipidine promotes fibroblast proliferation |
| Ca2+ through RyR—promotes differentiation in keratinocytes | ||
| Ca2+ through AE2—promotes keratinocytemigration | ||
| Ca2+ through TRP—affects proliferation, differentiation | ||
| Remodeling angiogenesis | H2S—increases blood perfusion around wounds | H2S—promotes angiogenesis |
| NO through iNOS—enhancing angiogenesis | ||
| Ca2+ blocking by azelnipidine promotes angiogenesis |
AE2, bicarbonate transporter type 2; CO, carbon monooxide; H2S, hydrogen sulfide; iNOS, inducible NO synthase; NO, nitric oxide; ROS, reactive oxygen species; RYR, ryanodine receptors; TRP, transient receptor potential channel; TRPV, vanilloid transient receptor potential channel.