Abstract
Ischemia/reperfusion (IR) injury, a main reason of mortality and morbidity worldwide, occurs in many organs and tissues. As a result of IR injury, senescent cells can accumulate in multiple organs. Increasing evidence shows that cellular senescence is the underlying mechanism that transforms an acute organ injury into a chronic one. Several recent studies suggest senescent cells can be targeted for the prevention or elimination of acute and chronic organ injury induced by IR. In this review, we concisely introduce the underlying mechanism and the pivotal role of premature senescence in the transition from acute to chronic IR injuries. Special focus is laid on recent advances in the mechanisms as well as on the basic and clinical research, targeting cellular senescence in multi-organ IR injuries. Besides, the potential directions in this field are discussed in the end. Together, the recent advances reviewed here will act as a comprehensive overview of the roles of cellular senescence in IR injury, which could be of great significance for the design of related studies, or as a guide for potential therapeutic target.