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Review
. 2021 Aug 16;22(16):8773.
doi: 10.3390/ijms22168773.

The Interplay between Autophagy and NLRP3 Inflammasome in Ischemia/Reperfusion Injury

Shuangyu Lv  1 , Huiyang Liu  1 , Honggang Wang  1
Affiliations
Review

The Interplay between Autophagy and NLRP3 Inflammasome in Ischemia/Reperfusion Injury

Shuangyu Lv et al. Int J Mol Sci. .

Abstract

Ischemia/reperfusion (I/R) injury is characterized by a limited blood supply to organs, followed by the restoration of blood flow and reoxygenation. In addition to ischemia, blood flow recovery can also lead to very harmful injury, especially inflammatory injury. Autophagy refers to the transport of cellular materials to the lysosomes for degradation, leading to the conversion of cellular components and offering energy and macromolecular precursors. It can maintain the balance of synthesis, decomposition and reuse of the intracellular components, and participate in many physiological processes and diseases. Inflammasomes are a kind of protein complex. Under physiological and pathological conditions, as the cellular innate immune signal receptors, inflammasomes sense pathogens to trigger an inflammatory response. TheNLRP3 inflammasome is the most deeply studied inflammasome and is composed of NLRP3, the adaptor apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and pro-caspase-1. Its activation triggers the cleavage of pro-interleukin (IL)-1β and pro-IL-18 mediated by caspase-1 and promotes a further inflammatory process. Studies have shown that autophagy and the NLRP3 inflammasome play an important role in the process of I/R injury, but the relevant mechanisms have not been fully explained, especially how the interaction between autophagy and the NLRP3 inflammasome participates in I/R injury, which remains to be further studied. Therefore, we reviewed the recent studies about the interplay between autophagy and the NLRP3 inflammasome in I/R injury and analyzed the mechanisms to provide the theoretical references for further research in the future.

Keywords: NLRP3 inflammasome; autophagy; ischemia/reperfusion injury; mitophagy; reactive oxygen species.

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Conflict of interest statement

The authors declare that there is no conflict of interest.

Figures

Figure 1
Figure 1
The general processes of macroautophagy, microautophagy and molecular chaperone-mediated autophagy.
Figure 2
Figure 2
The formation of the NLRP3 inflammasome.
Figure 3
Figure 3
The sketch of the process of ischemia-reperfusion injury.
Figure 4
Figure 4
The mechanisms of the interplay between autophagy and NLRP3 inflammasome.
See this image and copyright information in PMC

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