This reduces the autophagy and mitophagy dysfunctions that are reported to occur in type 2 diabetes mellitus patients (i.e., p53, p21, p16 proteins, and senescence-associated β galactosidase) and senescence-associated secretory phenotype (SASP) (i.e., matrix metalloproteinase 2 (MMP2), interleukin 6 (IL-6), and transforming growth factor (TGF) β) and increases the proliferation and migration rate of senescent VSMCs [23]. Here, IL6 is linked to diabetes mellitus.