Ischemia‐reperfusion injury (IRI) presents an intractable challenge for kidney donors, especially in the era of donation after circulatory death (DCD). Based on in‐depth studies of the renal IRI phenomenon, and the mechanisms involved, an increasing number of soluble mediators are being frequently associated with cellular dysfunction, cell death, and derivative rejection induced by oxidative stress, thus resulting in the failure of DCD kidney transplantation. Many of these soluble mediators are regulated by a spliced form of the X box‐binding protein 1 (XBP1s), a vital effector molecule for endoplasmic reticulum stress (ERS), or exert their functionality by influencing the expression of XBP1s. Owing to the existence of multiple XBP1s‐orchestrated soluble mediators, a variety of biological processes are known to be involved in the occurrence and development of IRI, thus manifesting as profound alterations in DCD kidney transplantation. In this review, we focus on the functionality of these XBP1s‐associated soluble mediators and their roles in oxidative stress following renal IRI. Our goal was to contribute to the advancement of strategies to prevent and treat IRI in the context of DCD kidney transplantation.
Zhang et al. (Thu,) studied this question.