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. 2021 Jan 7;13(2):180. doi: 10.3390/cancers13020180

Table 1.

Summary of studies about the role of HIF in cisplatin-induced AKI.

Number Model Strategies for HIF Regulation Involved HIF Isoforms Is HIF Activated or Inhibited Effects Underlying Mechanisms Reference
1 Rats cobalt HIF-1 and HIF-2, activated attenuate AKI apoptosis reduction via regulating mitochondrial pathways [16]
IRPTC, HIF-1 activated improve IRPTC survival
2 Rats; Carbon monoxide preconditioning HIF-1 activated attenuated AKI apoptosis reduction [17]
HCK-8 cells HIF-1 activated reduced apoptosis, increased proliferation
3 Mice; PHD inhibitor FG-4592 HIF-1 activated attenuated AKI apoptosis reduction, ameliorated inflammation [18]
HK-2 cells HIF-1 activated reduced apoptosis
4 Rats deferiprone HIF-1 activated attenuated AKI reduce apoptosis with increased Mcl1 and survivin expression [19]
5 Mice EC-specific
Phd2+/− mice
HIF-1, HIF-2 activated attenuated AKI induced antioxidative response [149]
6 HK-2 cells lentivirus-mediated HIF-1α-transfected hASCs HIF-1 activated reduced apoptosis and improved cellular morphology reduced apoptosis [150]
7 Mice lentivirus-mediated HIF-1α-transfected hASCs HIF-1 activated attenuated AKI reduced apoptosis, ameliorated inflammation [151]

IRPTC, immortalized rat proximal tubular cells; HCK-8, human renal proximal tubular cell line; HK-2, human proximal tubule epithelial cells; Mcl1, Myeloid cell leukemia-1; EC, endothelial cell; hASCs, Human adipose-derived stem cells.