TP53 and atherosclerosis: First, although JNJ-165 treatment suppressed ox-LDL-induced mitochondrial damage and inflammation in HAECs independent of p53, we cannot exclude the possible role of p53 in the protective effect of JNJ-165 against atherosclerosis by other mechanisms in different aortic cells, since this gene is involved in many signaling pathways that cause cell senescence, apoptosis and cell cycle arrest in the pathogenesis of atherosclerosis [35].