Reactive oxygen species formed during ischemic preconditioning may act as a trigger for cardioprotection by causing functional and structural alterations in subcellular organelles.
This review highlights the role of reactive oxygen species as triggers for both early and delayed ischemic preconditioning-induced cardioprotection.
Ischemic preconditioning (IPC) is an endogenous adaptive mechanism and is manifested by early and delayed phases of cardioprotection. Brief episodes of ischemia-reperfusion during IPC cause some subtle functional and structural alterations in sarcolemma, mitochondria, sarcoplasmic reticulum, myofibrils, glycocalyx, as well as nucleus, which render these subcellular organelles resistant to subsequent sustained ischemia-reperfusion insult. These changes occur in functional groups of various receptors, cation transporters, cation channels, and contractile and other proteins, and may explain the initial effects of IPC. On the other hand, induction of various transcriptional factors occurs to alter gene expression and structural changes in subcellular organelles and may be responsible for the delayed effects of IPC. Reactive oxygen species (ROS), which are formed during the IPC period, may cause these changes directly and indirectly and act as a trigger of IPC-induced cardioprotection. As ROS may be one of the several triggers proposed for IPC, this discussion is focused on the current knowledge of both ROS-dependent and ROS-independent mechanisms of IPC. Furthermore, some events, which are related to functional preservation of subcellular organelles, are described for a better understanding of the IPC phenomenon.
Saini et al. (Tue,) conducted a review in Ischemic preconditioning. Reactive oxygen species (ROS) was evaluated. Reactive oxygen species formed during ischemic preconditioning may act as a trigger for cardioprotection by causing functional and structural alterations in subcellular organelles.