Open Access
Wuhan Univ. J. Nat. Sci.
Volume 29, Number 1, February 2024
Page(s) 85 - 94
Published online 15 March 2024
  1. Dugar S, Choudhary C, Duggal A. Sepsis and septic shock: Guideline-based management[J]. Cleveland Clinic Journal of Medicine, 2020, 87(1): 53-64. [CrossRef] [PubMed] [Google Scholar]
  2. Shao Y, Saredy J, Yang W Y, et al. Vascular endothelial cells and innate immunity[J]. Arteriosclerosis, Thrombosis, and Vascular Biology, 2020, 40(6): e138-e152. [Google Scholar]
  3. Claser C, Nguee S Y T, Balachander A, et al. Lung endothelial cell antigen cross-presentation to CD8+T cells drives malaria-associated lung injury[J]. Nature Communications, 2019, 10(1): 4241. [NASA ADS] [CrossRef] [PubMed] [Google Scholar]
  4. Gould T J, Lysov Z, Liaw P C. Extracellular DNA and histones: Double-edged swords in immunothrombosis[J]. Journal of Thrombosis and Haemostasis, 2015, 13(Suppl 1): S82-S91. [CrossRef] [PubMed] [Google Scholar]
  5. Yang X, Li L, Liu J, et al. Extracellular histones induce tissue factor expression in vascular endothelial cells via TLR and activation of NF-κB and AP-1[J]. Thrombosis Research, 2016, 137: 211-218. [CrossRef] [PubMed] [Google Scholar]
  6. Kim S, Kim S Y, Pribis J P, et al. Signaling of high mobility group box 1 (HMGB1) through toll-like receptor 4 in macrophages requires CD14[J]. Molecular Medicine, 2013, 19: 88-98. [CrossRef] [PubMed] [Google Scholar]
  7. Grégoire M, Tadié J M, Uhel F, et al. Frontline Science: HMGB1 induces neutrophil dysfunction in experimental sepsis and in patients who survive septic shock[J]. Journal of Leukocyte Biology, 2017, 101(6): 1281-1287. [CrossRef] [PubMed] [Google Scholar]
  8. Barnay-Verdier S, Borde C, Fattoum L, et al. Emergence of antibodies endowed with proteolytic activity against High-mobility group box 1 protein (HMGB1) in patients surviving septic shock[J]. Cell Immunology, 2020, 347: 104020. [CrossRef] [Google Scholar]
  9. Andersson U, Tracey K J. HMGB1 is a therapeutic target for sterile inflammation and infection[J]. Annual Review of Immunology, 2011, 29: 139-162. [Google Scholar]
  10. Tsung A, Tohme S, Billiar T R. High-mobility group box-1 in sterile inflammation[J]. Journal of Internal Medicine, 2014, 276(5): 425-443. [Google Scholar]
  11. Yang H, Wang H, Chavan S S, et al. High mobility group box protein 1 (HMGB1): The prototypical endogenous danger molecule[J]. Molecular Medicine (Cambridge, Mass), 2015, 21(Suppl 1): S6-S12. [CrossRef] [PubMed] [Google Scholar]
  12. Deng M, Tang Y, Li W, et al. The endotoxin delivery protein HMGB1 mediates caspase-11-dependent lethality in sepsis[J]. Immunity, 2018, 49(4): 740-753e7. [CrossRef] [PubMed] [Google Scholar]
  13. Serhan C N. Treating inflammation and infection in the 21st century: New hints from decoding resolution mediators and mechanisms[J]. FASEB Journal, 2017, 31(4): 1273-1288. [CrossRef] [PubMed] [Google Scholar]
  14. VanPatten S, Al-Abed Y. High mobility group box-1 (HMGb1): Current wisdom and advancement as a potential drug target[J]. Journal of Medicinal Chemistry, 2018, 61(12): 5093-5107. [CrossRef] [PubMed] [Google Scholar]
  15. Pan Y, Wang D, Liu F. miR-146b suppresses LPS-induced M1 macrophage polarization via inhibiting the FGL2-activated NF-kappaB/MAPK signaling pathway in inflammatory bowel disease[J]. Clinics (Sao Paulo), 2022, 77: 100069. [CrossRef] [PubMed] [Google Scholar]
  16. Sobah M L, Liongue C, Ward A C. SOCS proteins in immunity, inflammatory diseases, and immune-related cancer[J]. Frontiers in Medicine (Lausanne), 2021, 8: 727987. [CrossRef] [Google Scholar]
  17. Ramírez L A, Pérez-Padilla E A, García-Oscos F, et al. A new theory of depression based on the serotonin/kynurenine relationship and the hypothalamicpituitary-adrenal axis[J]. Biomedica, 2018, 38(3): 437-450. [CrossRef] [PubMed] [Google Scholar]
  18. Tong L, Tang C, Cai C, et al. Upregulation of the microRNA rno-miR-146b-5p may be involved in the development of intestinal injury through inhibition of Kruppel-like factor 4 in intestinal sepsis[J]. Bioengineered, 2020, 11(1): 1334-1349. [CrossRef] [PubMed] [Google Scholar]
  19. Iorio M V, Croce C M. microRNA dysregulation in cancer: Diagnostics, monitoring and therapeutics. A comprehensive review[J]. EMBO Molecular Medicine, 2012, 4(3): 143-159. [CrossRef] [PubMed] [Google Scholar]
  20. Zhang Z, Chen L, Xu P, et al. Gene correlation network analysis to identify regulatory factors in sepsis[J]. Journal of Translational Medicine, 2020, 18(1): 381. [CrossRef] [PubMed] [Google Scholar]
  21. Zheng Y, Peng L, He Z, et al. Identification of differentially expressed genes, transcription factors, microRNAs and pathways in neutrophils of sepsis patients through bioinformatics analysis[J]. Cellular and Molecular Biology (Noisy-Le-Grand, France), 2022, 67(5): 405-420. [CrossRef] [PubMed] [Google Scholar]
  22. Comer B S, Camoretti-Mercado B, Kogut P C, et al. microRNA-146a and microRNA-146b expression and anti-inflammatory function in human airway smooth muscle[J]. American Journal of Physiology Lung Cellular and Molecular Physiology, 2014, 307(9): L727-L734. [CrossRef] [PubMed] [Google Scholar]
  23. Gao N, Dong L. MicroRNA-146 regulates the inflammatory cytokines expression in vascular endothelial cells during sepsis[J]. Pharmazie, 2017, 72(11): 700-704. [PubMed] [Google Scholar]
  24. Wang X, Yu Y. MiR-146b protect against sepsis induced mice myocardial injury through inhibition of Notch1[J]. Journal of Molecular Histology, 2018, 49(4): 411-417. [Google Scholar]
  25. Kanaan Z, Barnett R, Gardner S, et al. Differential microRNA (miRNA) expression could explain microbial tolerance in a novel chronic peritonitis model[J]. Innate Immunity, 2013, 19(2): 203-212. [CrossRef] [PubMed] [Google Scholar]
  26. Chen L, Yu L, Zhang R, et al. Correlation of microRNA-146a/b with disease risk, biochemical indices, inflammatory cytokines, overall disease severity, and prognosis of sepsis[J]. Medicine (Baltimore), 2020, 99(22): e19754. [CrossRef] [PubMed] [Google Scholar]
  27. Chen W, Liu L, Yang J, et al. MicroRNA-146b correlates with decreased acute respiratory distress syndrome risk, reduced disease severity, and lower 28-day mortality in sepsis patients[J]. Journal of Clinical Laboratory Analysis, 2020, 34(12): e23510. [CrossRef] [Google Scholar]
  28. Coopersmith C M, de Backer D, Deutschman C S, et al. Surviving sepsis campaign: Research priorities for sepsis and septic shock[J]. Intensive Care Medicine, 2018, 44(9): 1400-1426. [CrossRef] [PubMed] [Google Scholar]
  29. Singer M, Deutschman C S, Seymour C W, et al. The third international consensus definitions for sepsis and septic shock (sepsis-3)[J]. Metabolites, 2016, 315(8): 801-810. [Google Scholar]
  30. Feng J, Wang L, Feng Y, et al. Serum levels of angiopoietin 2 mRNA in the mortality outcome prediction of septic shock[J]. Experimental and Therapeutic Medicine, 2022, 23(5): 362. [CrossRef] [PubMed] [Google Scholar]
  31. Andersson U, Tracey K J. HMGB1 in sepsis[J]. Scandinavian Journal of Infectious Diseases, 2003, 35(9): 577-584. [CrossRef] [PubMed] [Google Scholar]
  32. Zheng Y J, Xu W P, Ding G, et al. Expression of HMGB1 in septic serum induces vascular endothelial hyperpermeability[J]. Molecular Medicine Reports, 2016, 13(1): 513-521. [CrossRef] [PubMed] [Google Scholar]
  33. Sundén-Cullberg J, Norrby-Teglund A, Rouhiainen A, et al. Persistent elevation of high mobility group box-1 protein (HMGB1) in patients with severe sepsis and septic shock[J]. Critical Care Medicine, 2005, 33(3): 564-573. [CrossRef] [PubMed] [Google Scholar]
  34. Unterwalder N, Meisel C, Savvatis K, et al. High-mobility group box-1 protein serum levels do not reflect monocytic function in patients with sepsis-induced immunosuppression[J]. Mediators of Inflammation, 2010, 2010: 745724. [CrossRef] [Google Scholar]
  35. Alpkvist H, Athlin S, Molling P, et al. High HMGB1 levels in sputum are related to pneumococcal bacteraemia but not to disease severity in community-acquired pneumonia[J]. Scientific Reports, 2018, 8(1): 13428. [NASA ADS] [CrossRef] [PubMed] [Google Scholar]
  36. Goldenberg N M, Steinberg B E, Slutsky A S, et al. Broken barriers: A new take on sepsis pathogenesis[J]. Science Translational Medicine, 2011, 3(88): 88ps25. [CrossRef] [PubMed] [Google Scholar]
  37. Joffre J, Hellman J, Ince C, et al. Endothelial responses in sepsis[J]. Am J Respir Crit Care Med, 2020, 202(3): 361-370. [Google Scholar]
  38. Vincent J L, Ince C, Pickkers P. Endothelial dysfunction: A therapeutic target in bacterial sepsis?[J]. Expert Opinion on Therapeutic Targets, 2021, 25(9): 733-748. [CrossRef] [PubMed] [Google Scholar]
  39. Zhang Y Y, Ning B T. Signaling pathways and intervention therapies in sepsis[J]. Signal Transduction and Targeted Therapy, 2021, 6(1): 407. [CrossRef] [PubMed] [Google Scholar]
  40. Pool R, Gomez H, Kellum J A. Mechanisms of organ dysfunction in sepsis[J]. Critical Care Clinics, 2018, 34(1): 63-80. [CrossRef] [PubMed] [Google Scholar]
  41. Nakamura T, Sato E, Fujiwara N, et al. Suppression of high-mobility group box-1 and receptor for advanced glycation end-product axis by polymyxin B-immobilized fiber hemoperfusion in septic shock patients[J]. Chemistry (Weinheim an Der Bergstrasse, Germany), 2011, 26(6): 546-549. [NASA ADS] [Google Scholar]
  42. Lee W, Kwon O K, Han M S, et al. Role of moesin in HMGB1-stimulated severe inflammatory responses[J]. Thromb Haemost, 2015, 114(2): 350-363. [CrossRef] [PubMed] [Google Scholar]
  43. Hill M, Tran N. miRNA interplay: Mechanisms and consequences in cancer[J]. Disease Models & Mechanisms, 2021, 14(4): dmm047662. [CrossRef] [PubMed] [Google Scholar]
  44. Ali Syeda Z, Langden S S S, Munkhzul C, et al. Regulatory mechanism of microRNA expression in cancer[J]. International Journal of Molecular Sciences, 2020, 21(5): E1723. [Google Scholar]
  45. Huang Y, Wang H, Wang Y, et al. Regulation and mechanism of miR-146 on renal ischemia reperfusion injury[J]. Pharmazie, 2018, 73(1): 29-34. [PubMed] [Google Scholar]
  46. Ghafouri-Fard S, Shoorei H, Taheri M. Non-coding RNAs participate in the ischemia-reperfusion injury[J]. Biomed Pharmacother, 2020, 129: 110419. [Google Scholar]
  47. Zhong L, Simard M J, Huot J. Endothelial microRNAs regulating the NF-kappaB pathway and cell adhesion molecules during inflammation[J]. FASEB J, 2018, 32(8): 4070-4084. [CrossRef] [MathSciNet] [PubMed] [Google Scholar]
  48. Olivieri F, Prattichizzo F, Giuliani A, et al. miR-21 and miR-146a: The microRNAs of inflammaging and age-related diseases[J]. Ageing Research Reviews, 2021, 70: 101374. [CrossRef] [PubMed] [Google Scholar]
  49. Vergadi E, Vaporidi K, Tsatsanis C. Regulation of endotoxin tolerance and compensatory anti-inflammatory response syndrome by non-coding RNAs[J]. Frontiers in Immunology, 2018, 9: 2705. [CrossRef] [PubMed] [Google Scholar]
  50. Benz F, Roy S, Trautwein C, et al. Circulating microRNAs as biomarkers for sepsis[J]. International Journal of Molecular Sciences, 2016, 17(1): E78. [Google Scholar]
  51. Dang C P, Leelahavanichkul A. Over-expression of miR-223 induces M2 macrophage through glycolysis alteration and attenuates LPS-induced sepsis mouse model, the cell-based therapy in sepsis[J]. PLoS One, 2020, 15(7): e0236038. [NASA ADS] [CrossRef] [PubMed] [Google Scholar]
  52. Gao M, Wang X, Zhang X, et al. Attenuation of cardiac dysfunction in polymicrobial sepsis by microRNA-146a is mediated via targeting of IRAK1 and TRAF6 expression[J]. Journal of Immunology, 2015, 195(2): 672-682. [Google Scholar]
  53. Laura B, Ferguson D A, McCall C E, et al. microRNA-146a and RBM4 form a negative feed-forward loop that disrupts cytokine mRNA translation following TLR4 responses in human THP-1 monocytes[J]. Immunology and Cell Biology, 2013, 91(8): 532-540. [CrossRef] [PubMed] [Google Scholar]
  54. Cheng H S, Sivachandran N, Lau A, et al. microRNA-146 represses endothelial activation by inhibiting proinflamma-tory pathways[J]. EMBO Molecular Medicine, 2013, 5(7): 1017-1034. [CrossRef] [PubMed] [Google Scholar]
  55. Wang Q, Li D, Han Y, et al. MicroRNA-146 protects A549 and H1975 cells from LPS-induced apoptosis and inflammation injury[J]. Journal of Biosciences, 2017, 42(4): 637-645. [CrossRef] [PubMed] [Google Scholar]
  56. Huang X, Zhu Z, Guo X, et al. The roles of microRNAs in the pathogenesis of chronic obstructive pulmonary disease[J]. International Immunopharmacology, 2019, 67: 335-347. [CrossRef] [PubMed] [Google Scholar]
  57. An R, Feng J, Xi C, et al. miR-146a attenuates sepsis-induced myocardial dysfunction by suppressing IRAK1 and TRAF6 via targeting ErbB4 expression[J]. Oxidative Medicine and Cellular Longevity, 2018, 2018: 7163057. [PubMed] [Google Scholar]
  58. Feng J, Zhu Y, Chen L, et al. Clinical significance of microRNA-146a in patients with ulcerative colitis[J]. Ann Clin Lab Sci, 2020, 50(4): 463-467. [PubMed] [Google Scholar]
  59. Li N, Wang J, Yu W, et al. MicroRNA146a inhibits the inflammatory responses induced by interleukin17A during the infection of helicobacter pylori[J]. Mol Med Rep 2019, 19(2): 1388-1395. [PubMed] [Google Scholar]
  60. Ge S, Wu X, Xiong Y, et al. HMGB1 inhibits HNF1A to modulate liver fibrogenesis via p65/miR-146b signaling[J]. DNA and Cell Biology, 2020, 39(9): 1711-1722. [CrossRef] [MathSciNet] [PubMed] [Google Scholar]
  61. Li Y, Zhang F, Cong Y, et al. Identification of potential genes and miRNAs associated with sepsis based on microarray analysis[J]. Mol Med Rep, 2018, 17(5): 6227-6234. [PubMed] [Google Scholar]
  62. Chen W, Ma X, Zhang P, et al. MiR-212-3p inhibits LPS-induced inflammatory response through targeting HMGB1 in murine macrophages[J]. Exp Cell Res, 2017, 350(2): 318-326. [CrossRef] [PubMed] [Google Scholar]

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