Cell pyroptosis in health and inflammatory diseases

Wu, Yongqi; Zhang, Jing; Yu, Sihui; Li, Yan; Zhu, Jinrong; Zhang, Kai; Zhang, Rongxin

doi:10.1038/s41420-022-00998-3

Cited by 51 publications

(34 citation statements)

References 91 publications

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“…Positive regulation of transcription, DNA-templated (GO:0045893), and cellular response to cytokine stimulus (GO:0071345) were among the top GO terms. Among the occurrence and progression of NAFLD and COVID-19, the release of cytokines and the activation of inflammatory response played essential roles in the process [33]. From the synthesis of cytokines to the proliferation of immune cells, DNA-templated transcription was the basis of all biological processes.…”

Section: Discussionmentioning

confidence: 99%

Systems biology approach reveals a common molecular basis for COVID-19 and non-alcoholic fatty liver disease (NAFLD)

et al. 2022

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Background Patients with non-alcoholic fatty liver disease (NAFLD) may be more susceptible to coronavirus disease 2019 (COVID-19) and even more likely to suffer from severe COVID-19. Whether there is a common molecular pathological basis for COVID-19 and NAFLD remains to be identified. The present study aimed to elucidate the transcriptional alterations shared by COVID-19 and NAFLD and to identify potential compounds targeting both diseases. Methods Differentially expressed genes (DEGs) for COVID-19 and NAFLD were extracted from the GSE147507 and GSE89632 datasets, and common DEGs were identified using the Venn diagram. Subsequently, we constructed a protein–protein interaction (PPI) network based on the common DEGs and extracted hub genes. Then, we performed gene ontology (GO) and pathway analysis of common DEGs. In addition, transcription factors (TFs) and miRNAs regulatory networks were constructed, and drug candidates were identified. Results We identified a total of 62 common DEGs for COVID-19 and NAFLD. The 10 hub genes extracted based on the PPI network were IL6, IL1B, PTGS2, JUN, FOS, ATF3, SOCS3, CSF3, NFKB2, and HBEGF. In addition, we also constructed TFs–DEGs, miRNAs–DEGs, and protein–drug interaction networks, demonstrating the complex regulatory relationships of common DEGs. Conclusion We successfully extracted 10 hub genes that could be used as novel therapeutic targets for COVID-19 and NAFLD. In addition, based on common DEGs, we propose some potential drugs that may benefit patients with COVID-19 and NAFLD.

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Section: Discussionmentioning

confidence: 99%

Systems biology approach reveals a common molecular basis for COVID-19 and non-alcoholic fatty liver disease (NAFLD)

et al. 2022

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“…According to recent studies, inflammasome activation with subsequent pyroptosis of the affected cells may contribute in an important manner to pathological changes in the joint [ 6 , 119 ]. It has been shown that the exposure of chondrocytes to proinflammatory molecules leads to NLRP3 inflammasome activation and subsequent pyroptosis of chondrocytes [ 120 ]. Pyroptosis may also be an important mechanism for OA-related pain as proinflammatory cytokines released from pyroptotic cells, particularly IL-1β, as well as depletion of the local population of macrophages, increase the excitability of nociceptors by altering the function of several neuronal ion channels and receptors in the nerve endings around the joint [ 121 , 122 ].…”

Section: Inflammasome Involvement In Primary Osteoarthritismentioning

confidence: 99%

The Role of Inflammasomes in Osteoarthritis and Secondary Joint Degeneration Diseases

Roškar

Hafner-Bratkovič

2022

Life

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Osteoarthritis is age-related and the most common form of arthritis. The main characteristics of the disease are progressive loss of cartilage and secondary synovial inflammation, which finally result in pain, joint stiffness, and functional disability. Similarly, joint degeneration is characteristic of systemic inflammatory diseases such as rheumatoid arthritis and gout, with the associated secondary type of osteoarthritis. Studies suggest that inflammation importantly contributes to the progression of the disease. Particularly, cytokines TNFα and IL-1β drive catabolic signaling in affected joints. IL-1β is a product of inflammasome activation. Inflammasomes are inflammatory multiprotein complexes that propagate inflammation in various autoimmune and autoinflammatory conditions through cell death and the release of inflammatory cytokines and damage-associated molecule patterns. In this article, we review genetic, marker, and animal studies that establish inflammasomes as important drivers of secondary arthritis and discuss the current evidence for inflammasome involvement in primary osteoarthritis. The NLRP3 inflammasome has a significant role in the development of secondary osteoarthritis, and several studies have provided evidence of its role in the development of primary osteoarthritis, while other inflammasomes cannot be excluded. Inflammasome-targeted therapeutic options might thus provide a promising strategy to tackle these debilitating diseases.

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“…Pyroptosis, a key component of innate immunity, plays a pivotal role in the occurrence and progression of autoimmune disorders. Excessive pyroptosis interrupts immune system homeostasis and thus initiates autoimmunity 98 . Uncontrolled release of inflammatory mediators from pyroptotic cells results in a hyper-activated immune system, which further exacerbates autoimmune diseases 99 .…”

Section: Sars-cov-2-induced Autoimmunity and Coagulopathymentioning

confidence: 99%

Pyroptotic cell death in SARS-CoV-2 infection: revealing its roles during the immunopathogenesis of COVID-19

Wang¹,

Chang²,

Zhang³

et al. 2022

Int. J. Biol. Sci.

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The rapid dissemination of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 , remains a global public health emergency. The host immune response to SARS-CoV-2 plays a key role in COVID-19 pathogenesis. SARS-CoV-2 can induce aberrant and excessive immune responses, leading to cytokine storm syndrome, autoimmunity, lymphopenia, neutrophilia and dysfunction of monocytes and macrophages. Pyroptosis, a proinflammatory form of programmed cell death, acts as a host defense mechanism against infections. Pyroptosis deprives the replicative niche of SARS-CoV-2 by inducing the lysis of infected cells and exposing the virus to extracellular immune attack. Notably, SARS-CoV-2 has evolved sophisticated mechanisms to hijack this cell death mode for its own survival, propagation and shedding. SARS-CoV-2-encoded viral products act to modulate various key components in the pyroptosis pathways, including inflammasomes, caspases and gasdermins. SARS-CoV-2-induced pyroptosis contriubtes to the development of COVID-19-associated immunopathologies through leakage of intracellular contents, disruption of immune system homeostasis or exacerbation of inflammation. Therefore, pyroptosis has emerged as an important mechanism involved in COVID-19 immunopathogenesis. However, the entangled links between pyroptosis and SARS-CoV-2 pathogenesis lack systematic clarification. In this review, we briefly summarize the characteristics of SARS-CoV-2 and COVID-19-related immunopathologies. Moreover, we present an overview of the interplay between SARS-CoV-2 infection and pyroptosis and highlight recent research advances in the understanding of the mechanisms responsible for the implication of the pyroptosis pathways in COVID-19 pathogenesis, which will provide informative inspirations and new directions for further investigation and clinical practice. Finally, we discuss the potential value of pyroptosis as a therapeutic target in COVID-19. An in-depth discussion of the underlying mechanisms of COVID-19 pathogenesis will be conducive to the identification of potential therapeutic targets and the exploration of effective treatment measures aimed at conquering SARS-CoV-2-induced COVID-19.

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Cell pyroptosis in health and inflammatory diseases

Cited by 51 publications

References 91 publications

Systems biology approach reveals a common molecular basis for COVID-19 and non-alcoholic fatty liver disease (NAFLD)

Systems biology approach reveals a common molecular basis for COVID-19 and non-alcoholic fatty liver disease (NAFLD)

The Role of Inflammasomes in Osteoarthritis and Secondary Joint Degeneration Diseases

Pyroptotic cell death in SARS-CoV-2 infection: revealing its roles during the immunopathogenesis of COVID-19

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