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interestingly, Akt was not a direct target of H 2 S, rather its phosphorylation was a downstream effect of VEGFR2 activation (Tao, Liu et al

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CBS is also involved in angiogenesis, and silencing of this enzyme was seen to significantly decrease HUVEC proliferation, diminish the pro-angiogenic effects of VEGF, and reduce transcription of the VEGF receptor VEGF receptor 2 (VEGFR2) and neuropilin 1—both essential for endothelial function—whereas exogenous H 2 S administration using NaHS and GYY4137 reversed these effects by stabilizing the transcription factor specificity protein 1 through protein S-sulfhydration (Saha, Chakraborty et al