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One possible strategy is to enhance autologous plasma with recombinant neurotrophic factors such as IGF1 or BDNF [114, 298]

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226 Moreover, HIF activation promotes cell proliferation and inhibits apoptosis in renal IR-induced AKI, and these effects can be reversed by treatment with the -catenin inhibitor IWR-1-endo, indicating interaction between HIF and the Wnt/-catenin signaling pathway in providing renal protection

Importantly, mitochondria are not only targets but also regulators, as ROS or stress signals can shift YAP/TAZ localization and activity via mechanisms involving RhoA oxidation, MOB1 acetylation, or mitochondrial proteins, such as EFHD1 and MIGA-2 [18]

BMC Genom