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

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.

 

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Acute kidney injury (AKI) is a significant global health problem, and there is currently no effective drug available to eliminate AKI. The death of renal cells is a crucial factor in the development of AKI. Targeted therapy for tubular epithelial cell (TEC) death is a prominent area of research in AKI treatment. Various forms of cell death, including apoptosis, necrosis, ferroptosis, and pyroptosis, are involved in the occurrence and progression of AKI. This article specifically focuses on the role of pyroptosis in AKI.

The assembly and activation of the NLRP3 inflammasome play a pivotal role in initiating pyroptosis, and it is influenced by several factors such as the activation of the NF-κB signaling pathway, mitochondrial instability, and excessive endoplasmic reticulum (ER) stress. The activation of the NLRP3 inflammasome leads to the release of downstream inflammatory cytokines, which further promote pyroptosis and ultimately contribute to the development of AKI.

This paper aims to review the potential mechanisms of pyroptosis in AKI and explore potential effective inhibitors targeting various key components involved in this process. By identifying these targets and developing therapeutic strategies to modulate pyroptosis, it may be possible to discover novel treatments for intrinsic AKI.

The findings of this review have the potential to provide insights into the underlying mechanisms of AKI and identify therapeutic targets for future drug development. By understanding and targeting pyroptosis, researchers may be able to develop more effective strategies for the treatment of AKI.

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Pyroptosis Caspase