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Published on: November 3, 2023
Pathway network of pyroptosis and its potential inhibitors in acute kidney injury
Ning Li1, Yuru Wang2, Xinyue Wang2
1Institute of Disaster and Emergency Medicine, Tianjin University, Tianjin 300072, China; State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin 300350, China; Tianjin Key Laboratory of Disaster Medicine Technology, Tianjin 300072, China; Wenzhou Safety (Emergency) Institute, Tianjin University, Wenzhou 325000, China.
Abstract:
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.
Insights
Pyroptosis, a form of programmed cell death, plays a key role in acute kidney injury (AKI). Targeting pyroptosis pathways offers a promising therapeutic strategy for treating AKI and preventing renal cell death.
Area of Science:
- Nephrology
- Cell Biology
- Immunology
Background:
- Acute kidney injury (AKI) is a global health concern with limited effective treatments.
- Renal cell death, particularly tubular epithelial cell (TEC) death, is a primary driver of intrinsic AKI.
- Various cell death modalities, including apoptosis, necrosis, ferroptosis, and pyroptosis, contribute to AKI pathogenesis.
Purpose of the Study:
- To review the role of pyroptosis in the mechanisms of AKI.
- To identify potential therapeutic targets within the pyroptosis pathway for AKI treatment.
Main Methods:
- Literature review focusing on pyroptosis and its involvement in AKI.
- Analysis of the NLRP3 inflammasome pathway and its upstream regulators (NF-κB, mitochondrial dysfunction, ER stress).
- Examination of downstream inflammatory cytokines and their role in pyroptosis-induced AKI.
Main Results:
- NLRP3 inflammasome activation is a central event in pyroptosis during AKI.
- Upstream factors like NF-κB signaling, mitochondrial instability, and ER stress influence NLRP3 inflammasome assembly.
- Activated NLRP3 inflammasome triggers inflammatory responses leading to pyroptosis and AKI.
Conclusions:
- Pyroptosis is a significant contributor to AKI pathogenesis.
- Inhibiting key targets in the pyroptosis pathway presents a novel therapeutic avenue for AKI.
- Understanding pyroptosis mechanisms can lead to the development of improved AKI treatment strategies.
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