[1]
|
Hemenway, G. and Frishman, W.H. (2022) Therapeutic Implications of NLRP3-Mediated Inflammation in Coronary Artery Disease. Cardiology in Review, 30, 90-99. https://doi.org/10.1097/CRD.0000000000000391
|
[2]
|
Lee, H.E., Lee, J.Y., Yang, G., et al. (2019) Inhibition of NLRP3 Inflammasome in Tumor Microenvironment Leads to Suppression of Metastatic Potential of Cancer Cells. Scientific Reports, 9, Article No. 12277.
https://doi.org/10.1038/s41598-019-48794-x
|
[3]
|
Wang Z, Zhang S, Xiao Y, et al. (2020) NLRP3 Inflammasome and Inflammatory Diseases. Oxidative Medicine and Cellular Longevity, 2020, Article ID: 4063562. https://doi.org/10.1155/2020/4063562
|
[4]
|
Liu, D., Zeng, X., Li, X., et al. (2020) Advances in the Molecular Mechanisms
of NLRP3 Inflammasome Activators and Inactivators. Biochemical Pharmacology, 175, Article ID: 113863. https://doi.org/10.1016/j.bcp.2020.113863
|
[5]
|
Zhang, B., Wei, W. and Qiu, J. (2018) ALK Is Required for NLRP3 Inflammasome Activation in Macrophage. Biochemical and Biophysical Research Communications, 501, 246-252. https://doi.org/10.1016/j.bbrc.2018.04.226
|
[6]
|
Kelley, N., Jeltema, D., Duan, Y., et al. (2019) The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation. International Journal of Molecular Sciences, 20, 3328. https://doi.org/10.3390/ijms20133328
|
[7]
|
杨斯迪, 邓奇峰, 黄瑞, 吴淑燕. 炎性小体激活与细胞焦亡的研究进展[J]. 微生物与感染, 2017, 12(3): 192-196.
|
[8]
|
肖少波, 等. 细胞焦亡: 一种与炎症相关的细胞死亡[J]. 生命的化学, 2017, 37(3): 423-428.
|
[9]
|
刘超英, 等. 细胞焦亡与炎症发生研究进展[J]. 动物医学进展, 2017, 38(9): 101-104.
|
[10]
|
黄茂凌, 等. 细胞焦亡发生机制及其与相关疾病的研究进展[J]. 疑难病杂志, 2019, 18(7): 744-747.
|
[11]
|
祁会丽, 等. 细胞焦亡激活机制及相关疾病研究进展[J]. 中华实用诊断与治疗杂志, 2016, 30(5): 417-419.
|
[12]
|
Yang, J., Zhao, Y. and Feng, S. (2015) Non-Canonical Activation of Inflammatory Caspases by Cytosolic LPS in Innate Immunity. Current Opinion in Immunology, 32, 78-83. https://doi.org/10.1016/j.coi.2015.01.007
|
[13]
|
Cazzola, M. (2020) Myelodysplastic Syndromes. New England Journal of Medicine, 383, 1358-1374.
https://doi.org/10.1056/NEJMra1904794
|
[14]
|
Basiorka, A.A., McGraw, K.L., Eksioglu, E.A., et al. (2016) The NLRP3
Inflammasome Functions as a Driver of the Myelodysplastic Syndrome Phenotype. Blood, 128, 2960-2975. https://doi.org/10.1182/blood-2016-07-730556
|
[15]
|
王金霞, 刘爱飞, 李方林, 陈懿建. 炎症小体在恶性血液病发病中的作用[J]. 中国老年学杂志, 2017, 37(16): 4154-4156.
|
[16]
|
Sallman, D.A., Cluzeau, T., Basiorka, A.A., et al. (2016) Unraveling the Pathogenesis of MDS: The NLRP3 Inflammasome and Pyroptosis Drive the MDS Pheno-Type U. Frontiers in Oncology, 6, 151.
https://doi.org/10.3389/fonc.2016.00151
|
[17]
|
Zhong, C., Wang, R., Hua, M., et al. (2021) NLRP3 Inflammasome Promotes the Progression of Acute Myeloid Leukemia via IL-1β Pathway. Frontiers in Immunology, 12, 2113. https://doi.org/10.3389/fimmu.2021.661939
|
[18]
|
Sallman, D.A. and List, A. (2019) The Central Role of Inflam-matory Signaling in
the Pathogenesis of Myelodysplastic Syndromes. Blood, 133, 1039-1048. https://doi.org/10.1182/blood-2018-10-844654
|
[19]
|
Fleming, V., Hu, X., Weber, R., et al. (2018) Targeting My-eloid-Derived Suppressor Cells to Bypass Tumor-Induced Immunosuppression. Frontiers in Immunology, 9, 98. https://doi.org/10.3389/fimmu.2018.00398
|
[20]
|
Ehsan, N., Ali, M., Mohammad, S.P., et al. (2021) Role of Mye-loid-Derived Suppressor Cell (MDSC) in Autoimmunity and Its Potential as a Therapeutic Target. Inflammopharmacology, 29, 1307-1315.
https://doi.org/10.1007/s10787-021-00846-3
|
[21]
|
Li, L.H., Yu, R., Cai, T.G., et al. (2020) Effects of Immune Cells and Cytokines on Inflammation and Immunosuppression in the Tumor Microenvironment. International Immunopharmacology, 88, Article ID: 106939.
https://doi.org/10.1016/j.intimp.2020.106939
|
[22]
|
Barreyro, L., Chlon, T.M. and Starczynowski, D.T. (2018) Chronic Immune Response Dysregulation in MDS Pathogenesis. Blood, 132, 1553-1560. https://doi.org/10.1182/blood-2018-03-784116
|
[23]
|
Qi, X., Jiang, H.J. Liu, P., et al. (2021) Increased Mye-loid-Derived Suppressor Cells in Patients with Myelodysplastic Syndromes Suppress CD8+ T Lymphocyte Function through the STAT3-ARG1 Pathway. Leukemia & Lymphoma, 62, 218-223. https://doi.org/10.1080/10428194.2020.1817431
|
[24]
|
Braun, T., Carvalho, G., Coquelle, A., et al. (2006) NF-kappaB Constitutes a Potential Therapeutic Target
in High-Risk Myelodysplastic Syndrome. Blood, 107, 1156-1165. https://doi.org/10.1182/blood-2005-05-1989
|
[25]
|
Han, D., Tao, J., Fu, R., et al. (2020) Myeloid-Derived Suppressor Cell Cytokine Secretion as Prognostic Factor in Myelodysplastic Syndromes. Innate Immunity, 26, 703-715. https://doi.org/10.1177/1753425920961157
|
[26]
|
Ben-Neriah, Y. and Karin, M. (2011) Inflammation Meets Cancer, with NF-KB as the Matchmaker. Nature Immunology, 12, 715-723. https://doi.org/10.1038/ni.2060
|
[27]
|
Sallman, D.A., Tanaka, T.N., List, A., et al. (2017) SOHO State of the Art
Update and Next Questions: Biology and Treatment of Myelodysplastic Syndromes. Clinical Lymphoma, Myeloma and Leukemia, 17, 613-620.
https://doi.org/10.1016/j.clml.2017.09.018
|
[28]
|
Ward, G.A., McGraw, K.L., Abbas-Aghabababababababeh, F., et al. (2021) Oxidized Mitochondrial DNA Released after Inflammasome Activation Is a Disease Biomarker for Myelodysplastic Syndromes. Blood Advances, 5, 2216-2228. https://doi.org/10.1182/bloodadvances.2020003475
|
[29]
|
Chen, L., Huang, C.F., Li, Y.C., et al. (2018) Blockage of the NLRP3 Inflammasome by MCC950 Improves Anti-Tumor Immune Responses in Head and Neck Squamous Cell Carcinoma. Cellular and Molecular Life Sciences, 75, 2045-2058. https://doi.org/10.1007/s00018-017-2720-9
|
[30]
|
Shi, H., Qin, Y., Tian, Y., et al. (2022) Interleukin-1beta Triggers the Expansion of Circulating Granulocytic Myeloid-Derived Suppressor Cell Subset Dependent on Erk 1/2 Activation. Immunobiology, 227, 152-165.
https://doi.org/10.1016/j.imbio.2021.152165
|
[31]
|
Tu, S., Bhagat, G., Cui, G., et al. (2008) Overexpression of In-terleukin-1β Induces Gastric Inflammation and Cancer and Mobilizes Myeloid-Derived Suppressor Cells in Mice. Cancer Cell, 14, 408-419.
https://doi.org/10.1016/j.ccr.2008.10.011
|