While the specific mechanisms underlying endothelial dysfunction in CC may vary among the different pathological characteristics of MetS, but they converge on several common pathological pathways such as disturbances in both of the NO/Cyclic Guanosine Monophosphate (cGMP) and Ras homolog family member A (RhoA)/ Rho-associated coiled-coil containing protein kinase (ROCK) signaling pathways, imbalance of endothelium-derived vasoactive factors, alterations in sex hormone regulation, oxidative stress, and programmed cell death (Figure 1)
A systematic review on inter-individual differences in cisplatin-induced nephrotoxicity has recently pointed towards three genes ( SLC22A2 , and two DNA repair genes) that determine sensitivity, suggesting that patient-specific dose optimization can be applied according to the genetic makeup
Zuber V, Gill D, Ala-Korpela M, Langenberg C, Butterworth A, Bottolo L, et al
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