Pyroptosis in diabetic nephropathy

Mamun, Abdullah Al; Mimi, Anjuman Ara; Wu, Yanqing; Zaeem, Muhammad; Aziz, Abdul; Suchi, Suzia Aktar; Alyafeai, Eman; Munir, Fahad; Xiao, Jian

doi:10.1016/j.cca.2021.09.003

Cited by 46 publications

(30 citation statements)

References 138 publications

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“…Although targeting the NLRP3 inflammasome has to date been shown to be effective in slowing disease progression and onset, there are currently no approved treatments which can ablate and/or downregulate its activity, a consequence of side effects and increased susceptibility to infection ( Niu et al, 2019 ). Exploring novel therapeutics alongside further research into the specific targeting of NLRP3 inflammasome components will undeniably offer hope for treating NLRP3-inflammasome associated diseases, such as diabetic nephropathy ( Kim et al, 2015 ; Sha et al, 2017 ; Mugisho et al, 2018 ; International Diabetes Federation, 2019 ; Zhao et al, 2019 ; Sun et al, 2020 ; Wang et al, 2020 ; Al Mamun et al, 2021 ; Samsu, 2021 ; ClinicalTrials.gov, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

The Role of the NLRP3 Inflammasome in Mediating Glomerular and Tubular Injury in Diabetic Nephropathy

et al. 2022

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The NOD-like receptor protein 3 (NLRP3) inflammasome is a multi-protein signalling complex integral to the chronic inflammatory response, activated in response to sterile and non-sterile cellular damage. The assembly and activation of the NLRP3 inflammasome comprise a two-step process involving nuclear factor kappa B (NFkB)-mediated priming, followed by canonical, non-canonical or alternative signalling pathways. These result in the maturation and release of inflammatory cytokines interleukin 1 beta (IL1ß) and interleukin-18 (IL18), which are associated with chronic inflammatory conditions including diabetic kidney disease. Diabetic nephropathy is a condition affecting ∼40% of people with diabetes, the key underlying pathology of which is tubulointerstitial inflammation and fibrosis. There is growing evidence to suggest the involvement of the NLRP3 inflammasome in this chronic inflammation. Early deterioration of kidney function begins in the glomerulus, with tubular inflammation dictating the progression of late-stage disease. Priming and activation of the NLRP3 inflammasome have been linked to several clinical markers of nephropathy including proteinuria and albuminuria, in addition to morphological changes including mesangial expansion. Treatment options for diabetic nephropathy are limited, and research that examines the impact of directly targeting the NLRP3 inflammasome, or associated downstream components are beginning to gain favour, with several agents currently in clinical trials. This review will explore a role for NLRP3 inflammasome activation and signalling in mediating inflammation in diabetic nephropathy, specifically in the glomerulus and proximal tubule, before briefly describing the current position of therapeutic research in this field.

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Section: Discussionmentioning

confidence: 99%

The Role of the NLRP3 Inflammasome in Mediating Glomerular and Tubular Injury in Diabetic Nephropathy

et al. 2022

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“…Caspase-1, NLRP3, and ASC are known to be the important modulators in cell pyroptosis [ 29 , 30 ]. Meanwhile, IL-1 β is also a pyroptosis-related cytokine [ 31 , 32 ]. Caspase-1 was often upregulated during the onset of neuronal injury, suggesting that the promotion of pyroptosis might be associated with neuronal injury [ 33 , 34 ].…”

Section: Discussionmentioning

confidence: 99%

Quercetin Alleviates the Progression of Breast Cancer-Related Depression via Inhibiting the Pyroptosis and Promoting the Immune Response

Zhu

Yang

et al. 2022

Mediators of Inflammation

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Background. Breast cancer-related depression (BCRD) seriously inhibits the life quality of patients with breast cancer. The Xiaoyao Kangai Jieyu Formula is known to inhibit the progression of depression. However, the detailed function of the Xiaoyao Kangai Jieyu Formula in BCRD remains unclear. Methods. Network pharmacology was constructed to assess the downstream target of the Xiaoyao Kangai Jieyu Formula in BCRD. In addition, the tail suspension test, sucrose preference test, and forced swimming test were used to test the symptom of depression in mice. Fluoro-Jade B staining was performed to observe the structure of neurons. RT-qPCR and western blot were applied to evaluate mRNA and protein levels. Besides, ELISA was performed to test the inflammatory responses and the immune response-related cytokines. Results. Quercetin was identified as the key component of the Xiaoyao Kangai Jieyu Formula. Quercetin significantly inhibited BCRD-induced neuron pyroptosis via downregulation of PYD and card domain containing (ASC), NLR family pyrin domain containing 3 (NLRP3), and caspase-1, and quercetin could reverse BCRD-caused inhibition of neuron viability. Quercetin significantly attenuated the symptom of BCRD in mice, and it could reverse the contents of 5-hydroxytryptamine (5-HT), dopamine (DA), and neutrophil elastase (NE) in mice. Moreover, quercetin could promote the immune responses in xenograft mice via upregulation of interleukin- (IL-) 2, interferon-γ (IFN-γ), and IL-10. Conclusion. Quercetin, the active ingredient of the Xiaoyao Kangai Jieyu Formula, effectively mitigated the progression of BCRD by inhibiting pyroptosis, promoting immune response, and improving serum metabolism.

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“…The noncanonical inflammasome pathway is mediated by caspase-4/5/11. All of these proteins can cleave GSDMD, leading to the activation of pyroptosis signaling pathways [ 44 ]. First, caspase-4/5/11 can directly recognize cytosolic lipopolysaccharide (LPS) [ 45 ].…”

Section: Pyroptosismentioning

confidence: 99%

Pyroptosis and Sarcopenia: Frontier Perspective of Disease Mechanism

Jin

Xie

et al. 2022

Cells

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With global ageing, sarcopenia, as an age-related disease, has brought a heavy burden to individuals and society. Increasing attention has been given to further exploring the morbidity mechanism and intervention measures for sarcopenia. Pyroptosis, also known as cellular inflammatory necrosis, is a kind of regulated cell death that plays a role in the ageing progress at the cellular level. It is closely related to age-related diseases such as cardiovascular diseases, Alzheimer’s disease, osteoarthritis, and sarcopenia. In the process of ageing, aggravated oxidative stress and poor skeletal muscle perfusion in ageing muscle tissues can activate the nod-like receptor (NLRP) family to trigger pyroptosis. Chronic inflammation is a representative characteristic of ageing. The levels of inflammatory factors such as TNF-α may activate the signaling pathways of pyroptosis by the NF-κB-GSDMD axis, which remains to be further studied. Autophagy is a protective mechanism in maintaining the integrity of intracellular organelles and the survival of cells in adverse conditions. The autophagy of skeletal muscle cells can inhibit the activation of the pyroptosis pathway to some extent. A profound understanding of the mechanism of pyroptosis in sarcopenia may help to identify new therapeutic targets in the future. This review article focuses on the role of pyroptosis in the development and progression of sarcopenia.

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Pyroptosis in diabetic nephropathy

Cited by 46 publications

References 138 publications

The Role of the NLRP3 Inflammasome in Mediating Glomerular and Tubular Injury in Diabetic Nephropathy

The Role of the NLRP3 Inflammasome in Mediating Glomerular and Tubular Injury in Diabetic Nephropathy

Quercetin Alleviates the Progression of Breast Cancer-Related Depression via Inhibiting the Pyroptosis and Promoting the Immune Response

Pyroptosis and Sarcopenia: Frontier Perspective of Disease Mechanism

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