Article
Biochemistry & Molecular Biology
Roberta Gonnella, Maria Saveria Gilardini Montani, Luisa Guttieri, Maria Anele Romeo, Roberta Santarelli, Mara Cirone
Summary: This study demonstrates the crucial role of the IRE1α/XBP1 axis in the survival of PEL cells, with minor influence from PERK and ATF6, and the ability of the IRE1α/XBP1 axis to induce the release of IL-6, IL-10, and VEGF. Additionally, IRE1α/XBP1 inhibition reduces STAT3 phosphorylation and induces pro-survival autophagy in PEL cells, suggesting that targeting this axis may be a promising strategy against PEL cells.
Article
Cell Biology
Lin-Shuang Zhang, Jin-Sheng Zhang, Yue-Long Hou, Wei-Wei Lu, Xian-Qiang Ni, Fan Lin, Xiu-Ying Liu, Xiu-Jie Wang, Yan-Rong Yu, Mo-Zhi Jia, Chao-Shu Tang, Ling Han, San-Bao Chai, Yong-Fen Qi
Summary: Intermedin (IMD) protects against cardiac fibrosis by inhibiting NLRP3 inflammasome activation and endoplasmic reticulum stress (ERS). IMD treatment improves cardiac function and reduces myocardial interstitial collagen deposition.
Article
Cell Biology
Weijia Li, Xibo Zhao, Rujian Zhang, Jiabin Xie, Guangmei Zhang
Summary: This study aims to investigate the role of NLRP3 in cisplatin resistance in ovarian cancer. It was found that NLRP3 is overexpressed in ovarian cancer and is associated with poor survival. Silencing NLRP3 gene can inhibit the malignant process of cisplatin-resistant ovarian cancer cells.
MEDIATORS OF INFLAMMATION
(2023)
Article
Biochemistry & Molecular Biology
Qingqing Ke, Caifeng Shi, Yunhui Lv, Lulu Wang, Jing Luo, Lei Jiang, Junwei Yang, Yang Zhou
Summary: This study analyzed the anti-fibrotic and anti-inflammatory effects of the SGLT2 inhibitor dapagliflozin on renal alternations. It was found that dapagliflozin mitigated inflammation and accumulation of metabolites in fibrosis renal tissue through the modulation of metabolism and immune-responsive genes. The study also demonstrated that dapagliflozin blocked the activation of the NLRP3 inflammasome, protecting the kidney from fibrosis development. This research identifies a novel mechanism coupling metabolism and inflammation for the kidney benefits of SGLT2 inhibition.
Review
Neurosciences
Lorena de Mena, Joshua Lopez-Scarim, Diego E. Rincon-Limas
Summary: Nuclear depletion, abnormal modification, and cytoplasmic aggregation of TDP-43 are associated with TDP-43 proteinopathies, including ALS and FTLD. While ER stress and the UPR play important roles in TDP-43 pathology, discrepancies exist between findings from neuronal models and in vitro/in vivo TDP-43 models. Future research should focus on integrating methodologies and models to uncover the true nature of the relationship between TDP-43 and ER stress.
FRONTIERS IN MOLECULAR NEUROSCIENCE
(2021)
Review
Biochemistry & Molecular Biology
Barbara Colombini, Monica Dinu, Emanuele Murgo, Sofia Lotti, Roberto Tarquini, Francesco Sofi, Gianluigi Mazzoccoli
Summary: Ageing is a multifactorial physiological manifestation that is closely related to inflammation and the functioning of the biological clock.
Review
Biochemistry & Molecular Biology
Gregorio Bonsignore, Simona Martinotti, Elia Ranzato
Summary: The unfolded protein response (UPR) is an adaptive response triggered by endoplasmic reticulum (ER) stress for re-establishing protein homeostasis. Specific ER proteins mediate UPR activation by dissociating from chaperone Glucose-Regulated Protein 78 (GRP78). UPR can decrease ER stress, produce an ER adaptive response, block UPR if ER homeostasis is restored, or regulate apoptosis. This review focuses on molecules that target ER stress and demonstrate how UPR could be a new target in cancer treatment.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Biochemistry & Molecular Biology
Maggie Lam, Ashley Mansell, Michelle D. Tate
Summary: This review discusses the beneficial effects of targeting the NLRP3 inflammasome in silicosis, where inhibition of this inflammasome can eliminate inflammation and fibrosis. However, clinical studies are needed to explore the role of NLRP3 inflammasomes in the clinical setting and to identify biomarkers for early detection of silicosis.
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
(2022)
Review
Immunology
Bhesh Raj Sharma, Thirumala-Devi Kanneganti
Summary: The NLRP3 inflammasome plays diverse roles in cancer and metabolic diseases, being involved in the release of inflammatory cytokines and inflammatory cell death upon activation. While inflammatory cytokines contribute to chronic inflammation and disease pathogenesis, fine tuning NLRP3 activity is crucial for maintaining cellular health.
Article
Immunology
Zhe Song, Li Wang, Yongxia Cao, Zihan Liu, Mingliang Zhang, Zhizi Zhang, Shan Jiang, Ruifeng Fan, Ting Hao, Ruyue Yang, Bingshun Wang, Zhenzhen Guan, Lina Zhu, Zhentao Liu, Shuya Zhang, Liang Zhao, Zhihao Xu, Haiwei Xu, Guifu Dai
Summary: This study firstly reported that (8R-12S)-isoandrographolide (ISA) from Andrographis paniculata can reduce pulmonary inflammation and fibrosis by inhibiting NLRP3, improving silicosis. ISA administration alleviated lung injury, attenuated inflammatory response, EMT, and collagen deposition in silica-induced mice. Further studies confirmed that ISA inhibited the expressions of NLRP3 inflammasome-related proteins, leading to the reduction of inflammation and EMT.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2022)
Article
Agriculture, Multidisciplinary
Xiaona Gao, Shuhui Liu, Lei Tan, Chenchen Ding, Wentao Fan, Zhangshan Gao, Mengcong Li, Zhihui Tang, Yuting Wu, Lei Xu, Liping Yan, Yan Luo, Suquan Song
Summary: This study demonstrated that estrogen receptor alpha plays a role in negatively controlling hepatocyte pyroptosis by inhibiting NLRP3 inflammasome activation. Inhibiting pyroptosis was found to alleviate metabolic dysfunction, insulin resistance, and liver injury caused by ER alpha deletion. Additionally, treatment with a phytoestrogen could attenuate high-fat diet-induced liver lipid steatosis and inhibit NLRP3-GSDMD-mediated pyroptosis.
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
(2021)
Article
Medicine, Research & Experimental
Hung-Jen Shih, Chao-Yuan Chang, Chung-Howe Lai, Chun-Jen Huang
Summary: The NLRP3 inflammasome-related TGF-β/Smad signaling pathway plays a crucial role in IC/BPS, and modulation of this pathway, such as using curcumin, can effectively mitigate the sequelae of chronic inflammation-induced bladder injury.
BIOMEDICINE & PHARMACOTHERAPY
(2021)
Article
Biochemistry & Molecular Biology
Krishan Kumar Saini, Priyank Chaturvedi, Abhipsa Sinha, Manish Pratap Singh, Muqtada Ali Khan, Ayushi Verma, Mushtaq Ahmad Nengroo, Saumya Ranjan Satrusal, Sanjeev Meena, Akhilesh Singh, Sameer Srivastava, Jayanta Sarkar, Dipak Datta
Summary: Ferroptosis is a distinct form of programmed cell death characterized by iron-dependent accumulation of lipid peroxides. Therapy-resistant tumor cells are vulnerable to ferroptosis. Modulating the balance of unfolded protein response (UPR) in cancer cells to make them susceptible to ferroptotic cell death could be a promising therapeutic strategy.
Review
Immunology
Yi Xiao, Li Zhang
Summary: The NLRP3 inflammasome plays a crucial role in regulating host immune function and its activation leads to cell pyroptosis and inflammatory cytokine production, affecting the development of arthritis. Recent studies have investigated the impact of NLRP3 inflammasome-mediated pyroptosis on various forms of arthritis and explored intervention approaches targeting this process. These findings offer new insights for the clinical identification and treatment of arthritis.
FRONTIERS IN IMMUNOLOGY
(2023)
Article
Multidisciplinary Sciences
Peng Zhao, Ping Huang, Tongfu Xu, Xiaoxiang Xiang, Ying Sun, Jingqi Liu, Cheng Yan, Lei Wang, Jiamei Gao, Shang Cui, Xiangdong Wang, Lixing Zhan, Haiyun Song, Jingnan Liu, Wei Song, Yong Liu
Summary: The study identified a novel catabolic role of Ire1 in regulating lipid mobilization in Drosophila, showing that it acts through promoting Xbp1s-associated FoxO degradation and suppressing FoxO-dependent lipolytic programs. These findings provide new insights into Ire1's conserved regulation of lipid homeostasis.