Hydrogen sulfide reduces pyroptosis and alleviates ischemia-reperfusion-induced acute kidney injury by inhibiting NLRP3 inflammasome

Ni, Jindi; Jiang, Lijing; Shen, Guofeng; Xia, Zhuye; Zhang, Lu; Xu, Jing; Feng, Quanxia; Qu, Hongping; Xu, Fulin; Li, Xiang

doi:10.1016/j.lfs.2021.119466

Cited by 37 publications

(29 citation statements)

References 48 publications

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“…α-Klotho protein has a therapeutic activity in contrast-induced AKI by limiting NLRP3 inflammasome-mediated pyroptosis [ 29 ]. The increased NLRP3 expression and pyroptosis level in AKI patients indicated LPS-induced NLRP3-dependent pyroptosis in AKI., consistent with previous results [ 30 , 31 ].…”

Section: Discussionsupporting

confidence: 94%

Knocking down ETS Proto-oncogene 1 (ETS1) alleviates the pyroptosis of renal tubular epithelial cells in patients with acute kidney injury by regulating the NLR family pyrin domain containing 3 (NLRP3) transcription

et al. 2022

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Acute kidney injury (AKI) has a high mortality rate, but its pathogenesis remains unclear Lipopolysaccharide (LPS)-mediated renal tubular epithelial pyroptosis is involved in the pathogenesis of AKI. NLR family of pyrin domains containing 3 (NLRP3) plays an important role in pyroptosis. To further understand the transcriptional regulation mechanism of NLRP3, the peripheral blood of patients with AKI was analyzed in this study, showing that the levels of NLRP3 and cell pyroptosis in patients with AKI were significantly higher than those in normal controls. Furthermore, elevated levels of NLRP3 and cell pyroptosis were found in renal tubular epithelial cells after LPS treatment. Transcription factor ETS Proto-Oncogene 1 (ETS1) could bind to the upstream promoter transcription site of NLRP3 to transactivate NLRP3 in renal tubular epithelial cells. The cell pyroptosis level also decreased by knocking down ETS1. It is concluded that knocking down of ETS1 may reduce the renal tubular epithelial pyroptosis by regulating the transcription of NLRP3, thus relieving AKI. ETS1 is expected to be a molecular target for the treatment of AKI.

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Section: Discussionsupporting

confidence: 94%

Knocking down ETS Proto-oncogene 1 (ETS1) alleviates the pyroptosis of renal tubular epithelial cells in patients with acute kidney injury by regulating the NLR family pyrin domain containing 3 (NLRP3) transcription

et al. 2022

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“…5 A and B). Together, the high sensitivity of SNP-1 to HSNO in biological systems was fully demonstrated, since decreased HSNO levels resulting from H 2 S depletion in ischemia-reperfused kidneys [ 55 ] were accurately detected. Furthermore, only the increase of HSNO, but not the increase of NO alone, could improve the fluorescence intensity.…”

Section: Resultsmentioning

confidence: 99%

A novel fluorescent probe for real-time imaging of thionitrous acid under inflammatory and oxidative conditions

et al. 2022

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“… 23 Current studies have demonstrated that those therapeutic interventions targeting NLRP3‐mediated pyroptosis could inhibit inflammatory response so as to alleviate the damage of various target organs experiencing I/R. 7 , 8 , 9 In 2020, He et al 11 first reported that N‐acetylcysteine alleviated postresuscitation myocardial dysfunction through the inhibition of cell pyroptosis mediated by NLRP3 inflammasome activation in rats. Thus, NLRP3‐mediated pyroptosis could be a potential target for myocardial protection after resuscitation.…”

Section: Discussionmentioning

confidence: 99%

“…Cell pyroptosis, one novel form of programmed cell death characterized by plasma membrane rupture and inflammatory cytokine release, plays a key role in the development of regional ischemia/reperfusion (I/R) injury of various organs. 7 , 8 , 9 Studies have confirmed that cell pyroptosis is mainly induced by the NOD‐like receptor protein 3 (NLRP3)–caspase‐1 pathway, in which the NLRP3 inflammasome promotes the activation of pro‐caspase‐1 into caspase‐1, then cleaves the proinflammatory cytokines interleukin‐1β and interleukin‐18 and the pyroptotic substrate gasdermin D, and finally results in cell death and excessive release of interleukin‐1β and interleukin‐18. 10 In the setting of CA/CPR, one investigation has preliminarily demonstrated that cell pyroptosis induced by NLRP3 inflammasome was involved in the development of myocardial dysfunction after resuscitation.…”

mentioning

confidence: 99%

Tubastatin A Improves Post‐Resuscitation Myocardial Dysfunction by Inhibiting NLRP3‐Mediated Pyroptosis Through Enhancing Transcription Factor EB Signaling

Zhao

Jiang

et al. 2022

JAHA

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Background Myocardial dysfunction is the leading cause of early death following successful cardiopulmonary resuscitation (CPR) in people with cardiac arrest (CA), which is potentially driven by cell pyroptosis mediated by NOD‐like receptor pyrin domain 3 (NLRP3) inflammasome. Recently, histone deacetylase 6 (HDAC6) inhibition was shown to exert effective myocardial protection against regional ischemia/reperfusion injury. In this study, we investigated whether tubastatin A, a specific histone deacetylase 6 inhibitor, could improve postresuscitation myocardial dysfunction through the inhibition of NLRP3‐mediated cell pyroptosis and its modulation mechanism. Methods and Results Healthy male white domestic swine were used to establish the model of CA/CPR in vivo, and the H9c2 cardiomyocyte hypoxia/reoxygenation model was used to simulate the CA/CPR process in vitro. Consequently, tubastatin A inhibited NLRP3 inflammasome activation, decreased proinflammatory cytokines production and cell pyroptosis, and increased cell survival after hypoxia/reoxygenation in H9c2 cardiomyocytes in vitro. In addition, tubastatin A increased the acetylated levels of transcription factor EB and its translocation to the nucleus, and its protective effect above was partly abrogated by transcription factor EB short interfering RNA after hypoxia/reoxygenation in H9c2 cardiomyocytes. Similarly, tubastatin A promoted cardiac transcription factor EB nuclear translocation, inhibited NLRP3‐mediated cell pyroptosis, and mitigated myocardial dysfunction after CA/CPR in swine. Conclusions The inhibition of histone deacetylase 6 activity by tubastatin A limited NLRP3 inflammasome activation and cell pyroptosis probably through the enhancement of transcription factor EB signaling, and therefore improved myocardial dysfunction after CA/CPR.

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Hydrogen sulfide reduces pyroptosis and alleviates ischemia-reperfusion-induced acute kidney injury by inhibiting NLRP3 inflammasome

Cited by 37 publications

References 48 publications

Knocking down ETS Proto-oncogene 1 (ETS1) alleviates the pyroptosis of renal tubular epithelial cells in patients with acute kidney injury by regulating the NLR family pyrin domain containing 3 (NLRP3) transcription

Knocking down ETS Proto-oncogene 1 (ETS1) alleviates the pyroptosis of renal tubular epithelial cells in patients with acute kidney injury by regulating the NLR family pyrin domain containing 3 (NLRP3) transcription

A novel fluorescent probe for real-time imaging of thionitrous acid under inflammatory and oxidative conditions

Tubastatin A Improves Post‐Resuscitation Myocardial Dysfunction by Inhibiting NLRP3‐Mediated Pyroptosis Through Enhancing Transcription Factor EB Signaling

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