Hypoxia is a condition characterized by a lack of oxygen in cells and tissues that plays a crucial role in numerous pathological conditions. The key mechanism that regulates cellular processes in hypoxic conditions is the activation of hypoxia-inducible factors (HIFs). HIF is activated by sensitive cellular oxygen sensors, while activated HIF regulates a complex network of cellular signaling pathways that control adaptive responses to hypoxia. There are categorised three types of hypoxia and it’s parameters for acute, chronic, and intermittent hypoxia. Intermittent hypoxia (IH) involves cyclic shifts between hypoxic periods and reoxygenation periods. IH is present in specific pathological conditions like obstructive sleep apnea, while in other cases, it is a significant protective factor that notably enhances clinical outcomes. Intermittent hypoxia mediates neuroprotective and cardioprotective effects through modulating the inflammatory response by acting on the nuclear factor κB (NF-κB) signaling pathway, increasing the activity of the antioxidant system, adjusting cellular energy metabolism towards anaerobic glycolysis, preventing apoptosis, and activating other adaptive signaling pathways and genes. Various signaling pathways contribute to the development of protective mechanisms of intermittent hypoxia, with the primary mediators being HIF-1α, nuclear factor erythroid 2-related factor 2, NF-κB, erythropoietin, vascular endothelial growth factor, and others whose roles are elucidated in this thesis.