Mechanisms of miRNA-mediated cell death in renal ischemia reperfusion injury

MiRNAs, which are integral to the complex regulatory mechanisms governing gene expression, have emerged as critical contributors to the intricate interplay of physiological and pathological processes within the human body. Their roles transcend mere participation, establishing them as pivotal biomarkers for disease diagnosis, potential therapeutic targets, and prognostic indicators, with significant implications. This prominence is particularly evident in the context of renal transplantation, in which IRI poses a significant challenge. The IRI process, characterized by an exacerbated impairment of tissue and organ functionality upon the re-establishment of blood flow following a period of ischemia, causes cellular structural damage and cell death, thereby compromising the functional integrity of the graft. A network of regulatory pathways regulated by miRNAs is central to the pathological development of IRI. These miRNAs modulate various cell death mechanisms and associated processes, such as ferroptosis, apoptosis, autophagy, pyroptosis, and oxidative stress, all of which critically influence the development of renal IRI. This review aims to elucidate the essence of miRNA-regulated cell death mechanisms within the broader context of renal IRI. By elucidating the nuanced roles of miRNAs in regulating these cell death mechanisms, we hope to unveil new therapeutic avenues and prognostic potential. The potential of miRNAs as novel cell death agents highlights their significance in refining treatment strategies, providing new hope for the management and mitigation of renal IRI.