In a murine model of IRI-induced AKI which subsequently developed into CKD, two intravenous injections of HLSC-EVs interfered with CKD development by effectively reducing interstitial fibrosis, the infiltration of inflammatory cells, and by down-regulating the gene expression levels of pro-fibrotic and pro-inflammatory markers, such as α-Sma, Col1a1, Tumor Necrosis Factor-α (TNF-α) and interleukin-6 (IL-6) [44]. The gene discussed is ACTA1; the disease is chronic kidney disease.