Sirt1 protects the heart from I/R injury through multiple mechanisms. For example, Sirt1 suppresses ROS production, apoptosis and inflammation, whereas it also induces autophagy. The effect of Sirt1 is mediated through both protein deacetylation (post-translational modification) and transcription (such as modulation of FoxO).
ROS: reactive oxygen species; UPR: unfolded protein response; NF-κB: nuclear factor of κ light polypeptide gene enhancer in B-cells; XBP: X-box binding protein; Bcl-xL: B cell lymphoma like X; Bax: Bcl-2-associated X; MnSOD: manganese superoxide dismutase; Trx: thioredoxin; Rab7: Rab-protein 7; LC3-II: light chain 3-II; FoxO1: forkhead box O1; NAD: nicotinamide adenine dinucleotide; STACs: Sirt1-activating compounds.