Review
Immunology
Frederic Bornancin, Carien Dekker
Summary: This review focuses on the regulation of the NLRP3 inflammasome by phosphorylation and dephosphorylation, and discusses the kinases and phosphatases that have been reported to modulate NLRP3 activity. The aim is to integrate the current understanding and highlight potential gaps for further studies.
FRONTIERS IN IMMUNOLOGY
(2023)
Review
Cell Biology
Alexander N. R. Weber
Summary: The NLRP3 inflammasome plays a crucial role in human diseases, and recent research has explored the potential of targeting NLRP3 via BTK, providing a new approach for inflammatory treatment.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Review
Immunology
Han Cheng, Lingling Chen, Minchun Huang, Jin Hou, Zhifeng Chen, Xiaojun Yang
Summary: NLRP3 inflammasome plays a key role in radiation-induced tissue injury, but its potential value is not adequately recognized. Early intervention/prevention strategies targeting NLRP3 inflammasome may help resolve clinical problems caused by radiation.
FRONTIERS IN IMMUNOLOGY
(2022)
Article
Immunology
Lei Hua, Shuli Liang, Yinghua Zhou, Xinyi Wu, Haowei Cai, Zhuorong Liu, Yitao Ou, Yanhong Chen, Xiuhui Chen, Yuyun Yan, Dan Wu, Ping Sun, Wenhui Hu, Zhongjin Yang
Summary: Artemisitene, a derivative of artemisinin, has been discovered to have enhanced activity in inhibiting the NLRP3 pathway. It can effectively suppress the production of ROS and prevent the assembly and activation of NLRP3 inflammasome, thus inhibiting the production of inflammatory cytokines. In addition, artemisitene also blocks IL-1 beta secretion mediated by NLRC4 and AIM2 inflammasome and IL-6 production. It shows potential as a drug candidate for inflammatory disorders.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2022)
Article
Cell Biology
Mojca Trstenjak-Prebanda, Monika Biasizzo, Klemen Dolinar, Sergej Pirkmajer, Boris Turk, Veronique Brault, Yann Herault, Natasa Kopitar-Jerala
Summary: It has been found that increased expression of stefin B in macrophages can downregulate mitochondrial reactive oxygen species (ROS) generation, decrease inflammasome activation, increase autophagy, and potentially contribute to the development of new treatments for related diseases.
Article
Cell Biology
Li-Zhen Liao, Zhi-Chong Chen, Sui-Sui Wang, Wen-Bin Liu, Chang-Lin Zhao, Xiao-Dong Zhuang
Summary: The activation of NLRP3 inflammasome plays a role in the pathogenesis of cardiocytes aging, potentially through the generation of reactive oxygen species (ROS). This study suggests that targeting NLRP3 inflammasome or inhibiting ROS generation could be strategies to attenuate cardiocytes aging.
Article
Biochemistry & Molecular Biology
Ling-Ya Chiu, Duen-Yi Huang, Wan-Wan Lin
Summary: PARP-1 positively regulates NLRP3 inflammasome activation by increasing ROS production and interacting with TXNIP and NLRP3.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2022)
Article
Immunology
Junjun Guo, Meijuan Zhou, Man Zhao, Shuxian Li, Zhenya Fang, Anna Li, Meihua Zhang
Summary: Through the study, it was found that TIGAR is up-regulated under high glucose conditions in vivo and in vitro, and loss of TIGAR increases ROS levels in trophoblast cells, leading to phenotypic changes and inhibition of migration, invasion, and tube formation. This switch is caused by the activation of the NLRP3-ASC-caspase-1 signaling pathway, resulting in pyroptosis. These findings can be reversed by antioxidant treatment and receptor blockage. In conclusion, trophoblast pyroptosis is an upstream event of TIGAR deficiency-induced inflammation, which is promoted by ROS accumulation through NLRP3-ASC inflammasome.
FRONTIERS IN IMMUNOLOGY
(2023)
Article
Pharmacology & Pharmacy
Ge Zhang, He Chen, Yifan Guo, Wei Zhang, Qiuyu Jiang, Si Zhang, Liping Han, She Chen, Ruyi Xue
Summary: This study found that assembly of NLRP3 inflammasome in platelets is increased in CD patients and associated with platelet hyperactivity. Elevated levels of intracellular reactive oxygen species were observed in platelets from patients with active CD, along with increased exposure of P-selectin and fibrinogen binding.
FRONTIERS IN PHARMACOLOGY
(2021)
Review
Oncology
Xueyan Shi, Sichuang Tan, Sipin Tan
Summary: The NLRP3 inflammasome plays a crucial role in sepsis by promoting immune defense and inflammatory responses through its activation pathway.
MOLECULAR MEDICINE REPORTS
(2021)
Article
Immunology
You Zhou, Yongjun Chen, Xiaowu Zhong, Hongtao Xia, Mingcai Zhao, Mengyuan Zhao, Lei Xu, Xiaolan Guo, Chong-Ge You
Summary: The findings suggest that Lipoxin A4 (LXA4) can inhibit the activation of NLRP3 inflammasome induced by monosodium urate (MSU) crystals, thereby exerting anti-inflammatory effects and reducing joint inflammation.
FRONTIERS IN IMMUNOLOGY
(2022)
Article
Immunology
Yuhua Shi, Qian Lv, Mengjie Zheng, Hongxiang Sun, Fushan Shi
Summary: INF39 is a specific inhibitor for NLRP3 inflammasome activation, without affecting other inflammasomes. It exerts its anti-inflammatory effect by inhibiting the interaction of NEK7-NLRP3 and other downstream events.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Jieun Kim, Hyun-ju Lee, Seon Kyeong Park, Jin-Hee Park, Ha-Ram Jeong, Soojung Lee, Heeyong Lee, Eunyoung Seol, Hyang-Sook Hoe
Summary: The study demonstrated that donepezil significantly reduces LPS- and A beta-induced neuroinflammatory responses in vitro and in vivo, suggesting it may be a therapeutic agent for neuroinflammation-associated diseases such as Alzheimer's disease.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Immunology
Xinyue Hu, Yingchun Shen, Yilin Zhao, Ji Wang, Xin Zhang, Wei Tu, William Kaufman, Juntao Feng, Peisong Gao
Summary: The study found that cockroach allergen induces overexpression of Muc5ac in human bronchial epithelial cells and asthma mouse model. Aryl hydrocarbon receptor (AhR) and mitochondrial ROS-NLRP3 inflammasome play important roles in regulating Muc5ac expression and airway inflammation.
FRONTIERS IN IMMUNOLOGY
(2021)
Article
Cell Biology
Qiao Yu, Huiying Shi, Zhen Ding, Zhe Wang, Hailing Yao, Rong Lin
Summary: This study reveals that Tripartite motif (TRIM) 31 negatively regulates the activation of NLRP3 inflammasome in Helicobacter pylori (Hp)-associated gastritis. Results demonstrated that TRIM31 negatively regulates NLRP3 inflammasome activation through affecting reactive oxygen species (ROS) and autophagy in gastric epithelial cells.
CELL COMMUNICATION AND SIGNALING
(2023)
Article
Biochemistry & Molecular Biology
Xiao Jiang, Xinyi Wang, Xianming Ding, Mengjie Du, Boran Li, Xialian Weng, Jingzi Zhang, Lin Li, Rui Tian, Qi Zhu, She Chen, Liang Wang, Wei Liu, Lei Fang, Dante Neculai, Qiming Sun
Article
Immunology
Xuexiao Jin, Qin Xu, Chengfei Pu, Kaixiang Zhu, Cheng Lu, Yu Jiang, Lei Xiao, Yongmei Han, Linrong Lu
Summary: The study investigated the feasibility of using anti-CD19 CAR-T cell therapy for treating SLE in a mouse model. Results demonstrated that the therapy was effective in both preventing and treating the disease in the murine model, with better therapeutic efficiency observed in CAR-T cells with the 4-1BB costimulatory motif.
CELLULAR & MOLECULAR IMMUNOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Jinle Tang, Yingjie Wang, Huan Zhou, Yuxin Ye, Manisha Talukdar, Ziyang Fu, Zhihong Liu, Jihui Li, Dante Neculai, Jiali Gao, Hao Huang
BIOCHEMICAL JOURNAL
(2020)
Article
Multidisciplinary Sciences
Li Chen, Qiaoqiao Tong, Xiaowen Chen, Penglei Jiang, Hua Yu, Qianbing Zhao, Lingang Sun, Chao Liu, Bin Gu, Yuping Zheng, Lijiang Fei, Xiao Jiang, Wenjuan Li, Giacomo Volpe, Mazid Md Abdul, Guoji Guo, Jin Zhang, Pengxu Qian, Qiming Sun, Dante Neculai, Miguel A. Esteban, Chen Li, Feiqiu Wen, Junfeng Ji
Summary: The study reveals that Phc1 can stabilize pluripotency by independently activating Nanog transcription in pluripotency maintenance, apart from its canonical function in PRC1. Phc1 interacts with Nanog to stabilize genome-wide chromatin interactions of the Nanog locus for transcriptional activation. This finding adds to the understanding of PcG proteins' role in maintaining pluripotency.
NATURE COMMUNICATIONS
(2021)
News Item
Biochemistry & Molecular Biology
Yan Lu, Dante Neculai
Summary: The activation of NOD1/2 is linked to ER homeostasis through the bioactive metabolite sphingosine1-phosphate (S1P), providing a new insight into cellular signaling pathways.
Article
Multidisciplinary Sciences
Yuxian Guo, Yaru Liu, Shihao Zhao, Wangting Xu, Yiqing Li, Pengwei Zhao, Di Wang, Hongqiang Cheng, Yuehai Ke, Xue Zhang
Summary: Redox-dependent regulation plays a key role in the pathogenesis of acute lung injury, and the study demonstrates that Grx1-regulated S-glutathionylation controls macrophage inflammation and alleviates acute lung injury, revealing a molecular mechanism.
NATURE COMMUNICATIONS
(2021)
Article
Cell Biology
Sheng Chen, Wenyu Cui, Zhexu Chi, Qian Xiao, Tianyi Hu, Qizhen Ye, Kaixiang Zhu, Weiwei Yu, Zhen Wang, Chengxuan Yu, Xiang Pan, Siqi Dai, Qi Yang, Jiacheng Jin, Jian Zhang, Mobai Li, Dehang Yang, Qianzhou Yu, Quanquan Wang, Xiafei Yu, Wei Yang, Xue Zhang, Junbin Qian, Kefeng Ding, Di Wang
Summary: The tumor microenvironment (TME) is a unique niche where constant communication within and between intratumoral cellular compartments occurs, with intratumoral high potassium (K+) having a suppressive effect on T cells. However, the impact of this ionic disturbance on innate immunity, as a pan-cancer characteristic associated with local necrosis, is unknown. In this study, the researchers discovered that intratumoral high K+ suppresses the anti-tumor capacity of tumor-associated macrophages (TAMs). The inwardly rectifying K+ channel Kir2.1 was identified as a central modulator of TAM functional polarization in high K+ TME, and its conditional depletion led to TAM repolarization towards an anti-tumor state, thereby enhancing local anti-tumor immunity. Kir2.1 deficiency disrupted electrochemically dependent glutamine uptake, causing TAM metabolic reprogramming from oxidative phosphorylation to glycolysis. Blocking Kir2.1 attenuated both murine tumor and patient-derived xenograft growth. Overall, the findings suggest that Kir2.1 is a determinant and potential therapeutic target for restoring the anti-tumor capacity of TAMs within an ionic-imbalanced TME.
Article
Immunology
Yang Luo, Yunfeng Zong, Hanju Hua, Meiting Gong, Qiao Peng, Chen Li, Dante Neculai, Xun Zeng
Summary: This study developed an immune-related scoring system based on immune signatures to predict prognosis and immunotherapeutic outcomes in colorectal cancer (CRC). CD103(+)CD39(+) T cells were identified as an immune signature that could predict prognosis and responses to immune checkpoint blockade therapy in CRC.
FRONTIERS IN IMMUNOLOGY
(2022)
Article
Gastroenterology & Hepatology
Fei Zhang, Ling-Dong Xu, Qian Zhang, Ailian Wang, Xinyuan Yu, Shengduo Liu, Chu Chen, Shiying Wu, Jianping Jin, Aifu Lin, Dante Neculai, Bin Zhao, Xin-Hua Feng, Tingbo Liang, Pinglong Xu, Yao-Wei Huang
Summary: We identified 17 efficient anti-hepatitis E virus (HEV) drugs through high-throughput screening, which showed promising results in vitro and in vivo. These drugs target the proteostasis of the HEV replicase and exhibited superior efficacy compared to conventional antivirals. This study provides insights into the critical host-HEV interactions and lays the foundation for the development of clinically promising antivirals.
JOURNAL OF HEPATOLOGY
(2023)
Article
Cell Biology
Maomao Pu, Wenhui Zheng, Hongtao Zhang, Wei Wan, Chao Peng, Xuebo Chen, Xinchang Liu, Zizhen Xu, Tianhua Zhou, Qiming Sun, Dante Neculai, Wei Liu
Summary: This study found that lipophagy, the process of autophagosomes engulfing and degrading lipid droplets, is crucial for lipid and energy homeostasis. The lipid transfer protein ORP8 was found to be located on lipid droplets and mediates their encapsulation by autophagosomal membranes through direct interaction with LC3/GABARAPs. Phosphorylation of ORP8 by AMPK enhances its affinity for LC3/GABARAPs. Deletion or disruption of the ORP8-LC3/GABARAP interaction leads to lipid droplet accumulation and increased intracellular triglyceride.
Article
Cell Biology
Xinyi Wang, Xiao Jiang, Boran Li, Jiahua Zheng, Jiansheng Guo, Lei Gao, Mengjie Du, Xialian Weng, Lin Li, She Chen, Jingzi Zhang, Lei Fang, Ting Liu, Liang Wang, Wei Liu, Dante Neculai, Qiming Sun
Summary: The study reveals that the ER-phagy receptor FAM134B is acetylated by CBP acetyltransferase and phosphorylated by CAMKII, leading to the degradation of the endoplasmic reticulum (ER). On the other hand, SIRT7 deacetylates FAM134B to reduce its activity in ER degradation. This work provides mechanistic insights into how ER-phagy is regulated and controlled.
JOURNAL OF CELL BIOLOGY
(2023)
Article
Genetics & Heredity
Yuyi Ying, Lu Lu, Santasree Banerjee, Lizhen Xu, Qiang Zhao, Hao Wu, Ruiqi Li, Xiao Xu, Hua Yu, Dante Neculai, Yongmei Xi, Fan Yang, Jiale Qin, Chen Li