CCL2 and acute kidney injury: These cells upregulated Pdgfd, Kcnip4, Vcam1 and Ccl2, all known markers for fibrosis and inflammation (Seron et al., 1991; Ostendorf et al., 2012; Kirita et al., 2020), while pathway analysis showed activation of AP-1 and NF-kB pathways, both pathways that have been identified previously to play an important role in driving kidney fibrosis after AKI (Liu et al., 2014; Ferenbach and Bonventre, 2015; Nakagawa et al., 2016; Kitani et al., 2022).