Under hyperlipidemia, the inhibition of SIRT3 and the acetylation of mitochondrial protein leads to the excessive utilization of fatty acids as energy substrates in addition to excess oxygen consumption, in turn adversely affecting cardiac cells (Lawrence et al., 1998; Sack, 2012; Fukushima and Lopaschuk, 2016). Here, SIRT3 is linked to hyperlipidemia.