NLRP3 inflammasome-mediated endothelial cells pyroptosis is involved in decabromodiphenyl ethane-induced vascular endothelial injury

Zheng, Dan; Shi, Zhixiong; Yang, Man; Liang, Baolu; Zhou, Xianqing; Li, Jing; Sun, Zhiwei

doi:10.1016/j.chemosphere.2020.128867

Cited by 17 publications

(2 citation statements)

References 44 publications

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“…In the state of sustained hyperglycemia occurring under IR, endothelial reactive oxygen species (ROS) markedly increase, resulting but not limited to oxidative stress and chronic inflammation, which even cause apoptosis, pyroptosis, and necrosis. Pyroptosis, or caspase-1-dependent cell death, is a typical proinflammatory programmed endothelial cell death related to the development of obesity-associated inflammation, diabetes, and IR [ 11 , 12 , 13 , 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

SIRT3 Modulates Endothelial Mitochondrial Redox State during Insulin Resistance

et al. 2022

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Emerging evidence indicates that defects in sirtuin signaling contribute to impaired glucose and lipid metabolism, resulting in insulin resistance (IR) and endothelial dysfunction. Here, we examined the effects of palmitic acid (PA) treatment on mitochondrial sirtuins (SIRT2, SIRT3, SIRT4, and SIRT5) and oxidative homeostasis in human endothelial cells (TeloHAEC). Results showed that treatment for 48 h with PA (0.5 mM) impaired cell viability, induced loss of insulin signaling, imbalanced the oxidative status (p < 0.001), and caused negative modulation of sirtuin protein and mRNA expression, with a predominant effect on SIRT3 (p < 0.001). Restoration of SIRT3 levels by mimic transfection (SIRT3+) suppressed the PA-induced autophagy (mimic NC+PA) (p < 0.01), inflammation, and pyroptosis (p < 0.01) mediated by the NLRP3/caspase-1 axis. Moreover, the unbalanced endothelial redox state induced by PA was counteracted by the antioxidant δ-valerobetaine (δVB), which was able to upregulate protein and mRNA expression of sirtuins, reduce reactive oxygen species (ROS) accumulation, and decrease cell death. Overall, results support the central role of SIRT3 in maintaining the endothelial redox homeostasis under IR and unveil the potential of the antioxidant δVB in enhancing the defense against IR-related injuries.

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Section: Introductionmentioning

confidence: 99%

SIRT3 Modulates Endothelial Mitochondrial Redox State during Insulin Resistance

et al. 2022

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“…Cardiovascular endothelial cell injury induced by Decabromodiphenyl ethane (DBDPE) enhances NLRP3 and caspase-1 activity, yet no studies have covered the therapeutic implications of GSDMD in cardiovascular injury induced by air pollutants. 71 Lastly, GSDMD plays a role in vascular smooth muscle cells and cardiovascular injury. GSDMD specific deficiency in vascular smooth muscle cells alleviates abdominal aortic aneurysm (AAA) by reducing putrescine compound levels in the aorta.…”

Section: Overview Of Pyroptosis and Gasdermin-dmentioning

confidence: 99%

The Role of Gasdermin-D-Mediated Pyroptosis in Organ Injury and Its Therapeutic Implications

2023

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Gasdermin-D (GSDMD) belongs to the Gasdermin family (GSDM), which are pore-forming effector proteins that facilitate inflammatory cell death, also known as pyroptosis. This type of programmed cell death is dependent on inflammatory caspase activation, which cleaves gasdermin-D (GSDMD) to form membrane pores and initiates the release of pro-inflammatory cytokines. Pyroptosis plays an important role in achieving immune regulation and homeostasis within various organ systems. The role of GSDMD in pyroptosis has been extensively studied in recent years. In this review, we summarize the role of GSDMD in cellular and organ injury mediated by pyroptosis. We will also provide an outlook on GSDMD therapeutic targets in various organ systems.

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