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

• Published in: Pharmacological research 2022-01, Vol.175, p.106033-106033, Article 106033
• Main Authors: Li, Ning, Wang, Yuru, Wang, Xinyue, Sun, Na, Gong, Yan-Hua
• Format: Article
• Language: English
• Subjects: Acute kidney injury; Acute Kidney Injury - drug therapy; Acute Kidney Injury - metabolism; Animals; Humans; NLRP3 inflammasome; Pyroptosis; Pyroptosis inhibitor; Signal Transduction; Signaling pathway
• ISSN: 1043-6618; 1096-1186
• DOI: 10.1016/j.phrs.2021.106033

Acute kidney injury (AKI) is a worldwide problem, and there is no effective drug to eliminate AKI. The death of renal cells is an important pathological basis of intrinsic AKI. At present, targeted therapy for TEC death is a research hotspot in AKI therapy. There are many ways of cell death involved in the occurrence and development of AKI, such as apoptosis, necrosis, ferroptosis, and pyroptosis. This article mainly focuses on the role of pyroptosis in AKI. The assembly and activation of NLRP3 inflammasome is a key event in the occurrence of pyroptosis, which is affected by many factors, such as the activation of the NF-κB signaling pathway, mitochondrial instability and excessive endoplasmic reticulum (ER) stress. The activation of NLRP3 inflammasome can trigger its downstream inflammatory cytokines, which will lead to pyroptosis and eventually induce AKI. In this paper, we reviewed the possible mechanism of pyroptosis in AKI and the potential effective inhibitors of various key targets in this process. It may provide potential therapeutic targets for novel intrinsic AKI therapies based on pyroptosis, so as to develop better therapeutic strategies. [Display omitted] This review mainly describes the possible signaling pathways of pyroptosis in acute kidney injury, focusing on the potential effective inhibitors of each molecular target in these signaling pathways.