Figure 8. Proposed model for the CDK5-mediated cell recovery of kidney tubular cells from Hx–Hp/Nx damage. (A) Under Nx conditions, CDK5 maintains a binding equilibrium between both partners p35/p25 and cyclin I signaling to cell survival. (B) Hx–Hp/Nx conditions would produce a decrease in the cyclin I protein levels to favor the formation of the CDK5/p35 complex. These changes would lead to the loss of pro-survival signaling induced by the CDK5/cyclin I complex. (C) Under Hx–Hp/Nx conditions, treatment with the CDK5 inhibitors would affect the CDK5/p35 complex without affecting the activity of the CDK5/cyclin I complex. This differential inhibition would promote the degradation of p35, the stabilization of the CDK5/cyclin I complex, and the engagement of a cell survival program.