Pathway network of pyroptosis and its potential inhibitors in acute kidney injury

Acute kidney injury (AKI) is a global health issue, and currently, there are no effective drugs available to cure it. The death of renal cells is a critical pathological factor in the development of intrinsic AKI. Targeted therapies aimed at preventing tubular epithelial cell (TEC) death have become a significant area of research in AKI treatment. Various forms of cell death, including apoptosis, necrosis, ferroptosis, and pyroptosis, play roles in the onset and progression of AKI. This article focuses specifically on the role of pyroptosis in AKI. The assembly and activation of the NLRP3 inflammasome are central to the occurrence of pyroptosis, influenced by factors such as NF-κB signaling pathway activation, mitochondrial instability, and excessive endoplasmic reticulum (ER) stress. Activation of the NLRP3 inflammasome triggers downstream inflammatory cytokines, leading to pyroptosis and ultimately contributing to AKI. This paper reviews the potential mechanisms of pyroptosis in AKI and explores effective inhibitors targeting key points in this process. These findings may offer novel therapeutic targets for developing intrinsic AKI treatments Ac-FLTD-CMK based on pyroptosis, paving the way for improved therapeutic strategies.