Experimental study reveals unaffected procoagulant platelet formation after SIRT3 deletion in mice, suggesting distinct mechanisms regulate platelet mitochondrial permeability.
deletion did not affect the generation of procoagulant platelets in response to strong dual agonist stimulation. These findings indicate that, despite its role in regulating mPTP opening in nucleated cells, platelet SIRT3 is not required for procoagulant platelet formation, suggesting that platelets rely on distinct mechanisms for mPTP regulation.
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Bael et al. (2026) studied this question.
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