CsA-induced inflammation, vascular resistance, nitric oxide production, vasopressor, fibrosis, and kidney injury were mediated by significant (p < 0.05) increases in the expression of nuclear factor kappa B (NF-kB), endothelin type A-receptor (ETA-R), inducible nitric oxide synthase (iNOS), angiotensin type 1-receptor (AT1-R), cellular fibronectin (cFN), kidney injury molecule-1 (Kim-1), and neutrophil gelatinase-associated lipocalin (NGAL) compared with the control group (Figure 4B–H). Here, HAVCR1 is linked to injury.