Patients with preeclampsia have augmented placental senescence compared to normal pregnant women as evidenced by telomere shortening in trophoblasts [82], while other studies have shown the upregulation of protein and gene expression of senescence-associated secretory phenotype (SASP) components including p16, p21, p53, IL-6, IL-8, plasminogen activator inhibitor-1 (PAI-1), and monocyte chemotactic protein-1 (MCP-1) in the placenta from preeclamptic patients compared to normotensive controls [83–86]. Here, CCL2 is linked to preeclampsia.