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Scheme illustrating prothrombotic effects of Sirt3 deficiency. Upon pro-inflammatory stimuli such as bacterial endotoxins (e.g. LPS) or oxLDL known to trigger human atherothrombotic events, endogenous Sirt3 protects neutrophils from NET formation (left). In contrast, absence of Sirt3 favours NETs, thereby accelerating clotting and increasing clot firmness (right) in mice. In patients with STEMI, SIRT3 transcription levels are reduced.
