Spinster homolog 2 (SPNS2) deficiency drives endothelial cell senescence and vascular aging via promoting pyruvate metabolism mediated mitochondrial dysfunction.

In addition, the mRNA level of senescence markers, such as KI67 and Lamin B1, and the protein level of Lamin B1 showed a decreasing trend in HUVECs after NAC treatment compared to those in HUVECs without NAC treatment (Figure S4 D, 4 J).

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Notably, ATP and acetyl-CoA levels in SPNS2 knockdown cells showed an increasing trend following PKM siRNA treatment (Fig. 5 N–Q), which may partly be because of the restoration of mitochondrial function.

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