ALAD and endothelial dysfunction: Finally, analysis of processes involved in the regulation of ageing, specific for sex of mice and specific for E3L.CETP and separately for C57BL/6J mice, revealed additional DEPs which deficiency leads to endothelial dysfunction development associated with increased oxidative stress, e.g. decreased antioxidant enzymes: peroxiredoxins—Prdx6, Prdx2, Prdx1, catalase or glutamate-cysteine ligase modifier subunit and delta-aminolevulinic acid dehydratase [85–88].