Pyroptosis-Related Inflammasome Pathway: A New Therapeutic Target for Diabetic Cardiomyopathy

Cai, Zhengyao; Yuan, Suxin; Luan, Xingzhao; Feng, Jian; Deng, Li; Zuo, Yumei; Li, Jiafu

doi:10.3389/fphar.2022.842313

Cited by 23 publications

(24 citation statements)

References 126 publications

(150 reference statements)

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“…Enhancing antioxidant defense may protect against diabetes-induced cardiac dysfunction ( 31 ). As one of the most important transcription factors, Nrf2 exerts antioxidant and anti-apoptotic effects by activating multiple antioxidant genes, including HO-1 and NQO1 ( 6 , 32 ). Our study showed that hyperglycemia increased ROS and MDA levels in vivo .…”

Section: Discussionmentioning

confidence: 99%

“…The underlying mechanisms of hyperglycemia-induced myocardial injury include cardiac inflammation, increased reactive oxygen species (ROS), interstitial fibrosis, and cardiac cell apoptosis ( 2 , 5 ). Such adverse reactions induce structural remodeling and affect heart diastolic function ( 6 ). Therefore, pharmacological inhibition of inflammation, ROS, and cell apoptosis has been proven to confer cardioprotection.…”

Section: Introductionmentioning

confidence: 99%

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Naringenin ameliorates myocardial injury in STZ-induced diabetic mice by reducing oxidative stress, inflammation and apoptosis via regulating the Nrf2 and NF-κB signaling pathways

Wang

Sun

et al. 2022

Front. Cardiovasc. Med.

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Diabetes-induced myocardial damage leads to diabetic cardiomyopathy and is closely associated with the generation of oxidative stress and inflammation. Naringenin (NG) exhibits antioxidant and anti-inflammatory effects. However, whether NG has cardioprotective effects against diabetic cardiomyopathy by regulating oxidative stress and inflammation remains unknown. This study investigated the effect of NG on diabetic cardiomyopathy based on an analysis of streptozotocin (STZ)-induced type 1 diabetic mice. The results indicated that NG reduced cardiac fibrosis and cardiomyocyte apoptosis in this diabetic model, accompanied by reduced blood glucose. NG inhibited pro-inflammatory cytokines, the level of reactive oxygen species and the expression of nuclear factor kappa-B (NF-κB), whereas the expression of antioxidant enzymes and nuclear factor erythroid 2-related factor 2 (Nrf2) were greatly enhanced by NG. Furthermore, in high glucose-treated H9C2 myocardial cells, NG effectively reduced cell apoptosis by inhibiting the formation of reactive oxygen species and pro-inflammatory cytokines. NG's antioxidant and anti-inflammatory activities were mechanistically associated with NF-κB inhibition and Nrf2 activation in animal and cell experiments. Data analysis showed that NG could regulate Nrf2 and NF-κB pathways to protect against diabetes-induced myocardial damage by reducing oxidative stress and inhibiting inflammation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Naringenin ameliorates myocardial injury in STZ-induced diabetic mice by reducing oxidative stress, inflammation and apoptosis via regulating the Nrf2 and NF-κB signaling pathways

Wang

Sun

et al. 2022

Front. Cardiovasc. Med.

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“…Programmed cell death is a hot issue in biological and medical research, and targeting the cell death process is a common approach in tumor therapy. However, current compounds that induce programmed death are only effective against certain tumor cells, and different types of cancers seem to have different sensitivities to programmed death ( 177 – 179 ). Efforts to understand the sensitivity of different tissue tumors to programmed death are important for the practice of clinical application of programmed death in tumor therapy.…”

Section: Conclusion and Prospectsmentioning

confidence: 99%

Ferroptosis, necroptosis, and pyroptosis in the occurrence and development of ovarian cancer

Zhang

Liu

2022

Front. Immunol.

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Ovarian cancer (OC) is one of the most common malignancies that causes death in women and is a heterogeneous disease with complex molecular and genetic changes. Because of the relatively high recurrence rate of OC, it is crucial to understand the associated mechanisms of drug resistance and to discover potential target for rational targeted therapy. Cell death is a genetically determined process. Active and orderly cell death is prevalent during the development of living organisms and plays a critical role in regulating life homeostasis. Ferroptosis, a novel type of cell death discovered in recent years, is distinct from apoptosis and necrosis and is mainly caused by the imbalance between the production and degradation of intracellular lipid reactive oxygen species triggered by increased iron content. Necroptosis is a regulated non-cysteine protease–dependent programmed cell necrosis, morphologically exhibiting the same features as necrosis and occurring via a unique mechanism of programmed cell death different from the apoptotic signaling pathway. Pyroptosis is a form of programmed cell death that is characterized by the formation of membrane pores and subsequent cell lysis as well as release of pro-inflammatory cell contents mediated by the abscisin family. Studies have shown that ferroptosis, necroptosis, and pyroptosis are involved in the development and progression of a variety of diseases, including tumors. In this review, we summarized the recent advances in ferroptosis, necroptosis, and pyroptosis in the occurrence, development, and therapeutic potential of OC.

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“…Pyroptosis is a type of inflammatory programmed cell death. It is mediated by gasdermin (GSDM) and is characterized by inflammasome activation, caspase activation, and formation of cell membrane pores [15][16][17]. GSDMDmediated pyroptosis has a role in the occurrence and development of diabetic cardiomyopathy and diabetic nephropathy [15,18,19].…”

Section: Introductionmentioning

confidence: 99%

“…It is mediated by gasdermin (GSDM) and is characterized by inflammasome activation, caspase activation, and formation of cell membrane pores [15][16][17]. GSDMDmediated pyroptosis has a role in the occurrence and development of diabetic cardiomyopathy and diabetic nephropathy [15,18,19]. Although the relationship between diabetic vascular injury and pyroptosis is not well established, current studies prompted us to clarify the significance of pyroptosis in diabetic vascular injury, the initial engine in pathological progress of diabetes.…”

Section: Introductionmentioning

confidence: 99%

Recurrent Hypoglycemia Impaired Vascular Function in Advanced T2DM Rats by Inducing Pyroptosis

Luo

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. Hypoglycemia is a dangerous side effect of intensive glucose control in diabetes. Even though it leads to adverse cardiovascular events, the effects of hypoglycemia on vascular biology in diabetes have not been adequately studied. Methods. Aged Sprague-Dawley rats were fed a high-fat diet and given streptozotocin to induce type 2 diabetes mellitus (T2DM). Acute and recurrent hypoglycemia were then induced by glucose via insulin administration. Vascular function, oxidative stress, and pyroptosis levels in aortic tissue were assessed by physiological and biochemical methods. Results. Hypoglycemia was associated with a marked decrease in vascular function, elevated oxidative stress, and elevated pyroptosis levels in the thoracic aorta. The changes in oxidative stress and pyroptosis were greater in rats with recurrent hypoglycemia than in those with acute hypoglycemia. Conclusions. Hypoglycemia impaired vascular function in aged rats with T2DM by inducing pyroptosis. The extent of injury increased with the duration of blood glucose fluctuation.

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Pyroptosis-Related Inflammasome Pathway: A New Therapeutic Target for Diabetic Cardiomyopathy

Cited by 23 publications

References 126 publications

Naringenin ameliorates myocardial injury in STZ-induced diabetic mice by reducing oxidative stress, inflammation and apoptosis via regulating the Nrf2 and NF-κB signaling pathways

Naringenin ameliorates myocardial injury in STZ-induced diabetic mice by reducing oxidative stress, inflammation and apoptosis via regulating the Nrf2 and NF-κB signaling pathways

Ferroptosis, necroptosis, and pyroptosis in the occurrence and development of ovarian cancer

Recurrent Hypoglycemia Impaired Vascular Function in Advanced T2DM Rats by Inducing Pyroptosis

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