Furthermore, 3-MA, a classic autophagy inhibitor, could significantly reverse EP4 agonist-induced autophagy, and abrogate the ameliorating effects of EP4 agonist on the progression of AKI to CKD in vivo, as evidenced by alleviated kidney injury, reduced fibrotic area, downregulated expressions of fibrosis markers (fibronectin and α-SMA) and increased the pro-inflammatory M1 macrophages, and inhibited the anti-inflammatory M2 macrophages in IRI mice, compared with CAY10580-treated group though inducing lipophagy in macrophages (Figures 5A–E). The gene discussed is ACTA1; the disease is chronic kidney disease.