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RSS augmentation leverages controlled-release H 2 S/persulfide donors (including organelle-targeted chemotypes when appropriate) to stabilize redox-sensitive thiols via persulfidation and to recycle sulfenylated switches back to the signalling-competent state—dosed to local set-points to avoid off-target mitochondrial inhibition, hypotension, or interference with immune defence and guided by biomarkers such as nitrosothiols/persulfide load, peroxiredoxin redox state and compartment-targeted H 2 O 2 reporters to verify that NO and sulfur signalling are restored while nitrative and Fenton-linked chemistries are constrained (Filipovic et al

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The authors conclude that NMN supplementation might also be effective in human T2D patients [13]