Figure 1.

Representation of the cellular and molecular pathways of damage induced following a time course of hypoxia and ischemia–reperfusion cycle in different tissues. The activation of enzymatic and non-enzymatic sources of reactive oxygen species (ROS) is associated with the modulation of redox-sensitive transcriptional factors, such as the activation of nuclear factor (NF)-κB and inhibition of nuclear factor erythroid 2—related factor 2 (Nrf2). Both cellular pathways are implicated in the oxidative modifications or pro-inflammatory effects that can mediate structural or functional cardiovascular impairment.