mtDNA release is a marker of mitochondrial damage that was well‐established in AS pathogenesis.[23] Consistently, KEGG and GO enrichment analysis revealed robust downregulation of genes associated with mitochondrial structure and function in VSMCs from CKD/ApoE−/− mice (Figure 6F), suggesting that enhanced mitochondrial damage in VSMCs might be responsible for accelerated AS progression and plaque vulnerability. This evidence concerns the gene APOE and chronic kidney disease.