For example, Bdh1-knockout mice showed more severe ventricular remodeling and dysfunction after TAC/myocardial infarction (Uchihashi et al., 2017), whereas in the stress overload model, the Bdh1 overexpression attenuated cardiac remodeling and DNA damage, suggesting that increased ketone utilization was adaptive (Shimazu et al., 2013). Here, BDH1 is linked to myocardial infarction.