TP53BP1 and myocardial infarction: In line with a previous study linking ramipril to DNA damage repair after myocardial infarction (73), we observed that compared with sunitinib treatment, which promoted DNA damage, combined use of sunitinib and ramipril led to a significant decrease in γ-H2AX foci and a notable increase in 53BP1 foci in cardiac ECs (Figure 7, I and J); this suggested an increased DDR, which we showed to be regulated by SND1/UBE2N/RNF8/RNF168.