内脂素在脓毒症相关性脏器损伤中的作用及机制研究进展

doi:10.16352/j.issn.1001-6325.2022.08.1279

基础医学与临床 ›› 2022, Vol. 42 ›› Issue (8): 1279-1283.doi: 10.16352/j.issn.1001-6325.2022.08.1279

内脂素在脓毒症相关性脏器损伤中的作用及机制研究进展

匡重伸, 丛竹凯, 吴长毅, 杨宁, 宗亚楠, 郭向阳^*

北京大学第三医院麻醉科,北京 100191

收稿日期:2022-05-19 修回日期:2022-06-13 出版日期:2022-08-05 发布日期:2022-08-01
通讯作者: ^*puthmzk@hsc.pku.edu.cn
基金资助:
国家自然科学基金(81873726, 81971012); 北京大学临床+X青年专项(PKU2020LCXQ016)

Research progress on the role and mechanism of visfatin in sepsis-related organ injury

KUANG Zhong-shen, CONG Zhu-kai, WU Chang-yi, YANG Ning, ZONG Ya-nan, GUO Xiang-yang^*

Department of Anesthesiology, Peking University Third Hospital, Beijing 100191, China

Received:2022-05-19 Revised:2022-06-13 Online:2022-08-05 Published:2022-08-01
Contact: ^*puthmzk@hsc.pku.edu.cn

摘要/Abstract

摘要： 脓毒症(sepsis)是临床常见的急危重症,全身炎性反应(SIRS)是脓毒症发生的关键机制之一,内脂素(visfatin)作为一种重要的细胞因子,参与脓毒症引起的“炎症风暴”的发生发展。最近的临床及基础研究表明,内脂素在脓毒症的发生发展中起着重要作用,抑制内脂素的表达可改善脓毒症导致的系统炎性反应及肺、心脏、肝脏等重要脏器的损伤。结合目前的临床及基础研究结果分析,内脂素有望成为脓毒症疾病严重程度的评价指标以及潜在的临床干预靶点。

关键词: 内脂素, 脓毒症, 多器官功能障碍综合征

Abstract: Sepsis is a common acute and critical disease in clinic. Systemic inflammatory response (SIRS) is one of the key mechanisms for the occurrence of sepsis. Visfatin, as an important cytokine, is involved in the occurrence and development of “cytokines storm” caused by sepsis. Recent clinical and basic research have shown that visfatin plays an important role in the occurrence and development of sepsis, and inhibition of visfatin expression can improve the systemic inflammatory response and the damage of lung, heart, liver and other important organs caused by sepsis. Based on the analysis of current clinical and basic research results, visfatin are expected to become an indicator of the severity of sepsis and a potential target for clinical intervention.

Key words: visfatin, sepsis, MODS

中图分类号:

R363

匡重伸, 丛竹凯, 吴长毅, 杨宁, 宗亚楠, 郭向阳. 内脂素在脓毒症相关性脏器损伤中的作用及机制研究进展[J]. 基础医学与临床, 2022, 42(8): 1279-1283.

KUANG Zhong-shen, CONG Zhu-kai, WU Chang-yi, YANG Ning, ZONG Ya-nan, GUO Xiang-yang. Research progress on the role and mechanism of visfatin in sepsis-related organ injury[J]. Basic & Clinical Medicine, 2022, 42(8): 1279-1283.

参考文献 26

[1]	Braun DA. Retrospective review of the sepsis definition after publication of sepsis-3[J]. Am J Med, 2019, 132:382-384.
[2]	Karki R, Kanneganti TD. The ‘cytokine storm’:mole-cular mechanisms and therapeutic prospects[J]. Trends Immunol, 2021, 42:681-705.
[3]	Black WB, Zhang LY, Mak WS, et al. Engineering a nicotinamide mononucleotide redox cofactor system for biocatalysis[J]. Nature chemical biology, 2020, 16:87-94.
[4]	Managò A, Audrito V, Mazzola F, et al. Extracellular nicotinate phosphoribosyltransferase binds Toll like receptor 4 and mediates inflammation[J]. Nat Commun, 2019, 10:4116.doi:10.1038/s41467-019-12055-2.
[5]	Rongvaux A, Shea RJ, Mulks MH, et al. Pre-B-cell colony-enhancing factor, whose expression is up-regulated in activated lymphocytes, is a nicotinamide phosphoribosyltransferase, a cytosolic enzyme involved in NAD biosynthesis[J]. Eur J Immunol, 2002, 32:3225-3234.
[6]	Fukuhara A, Matsuda M, Nishizawa M, et al. Visfatin:a protein secreted by visceral fat that mimics the effects of insulin[J]. Science, 2005, 307:426-430.
[7]	Nowell M, Evans L, Williams A. PBEF/NAMPT/visfatin:a promising drug target for treating rheumatoid arthritis?[J]. Future Med Chem, 2012, 4:751-769.
[8]	Jia SH, Li Y, Parodo J, et al. Pre-B cell colony-enhancing factor inhibits neutrophil apoptosis in experimental inflammation and clinical sepsis[J]. J Clin Invest, 2004, 113:1318-1327.
[9]	Bruzzone S, Fruscione F, Morando S, et al. Catastrophic NAD+ depletion in activated T lymphocytes through Nampt inhibition reduces demyelination and disability in EAE[J]. PLoS One, 2009, 4:e7897.doi:10.1371/journal.pone.0007897.
[10]	Huffaker TB, Ekiz HA, Barba C, et al. A Stat1 bound enhancer promotes Nampt expression and function within tumor associated macrophages[J]. Nat Commun, 2021, 12:2620.doi:10.1038/s41467-021-22923-5.
[11]	Rotllan N, Camacho M, Tondo M, et al. Therapeutic potential of emerging NAD+-increasing strategies for cardiovascular diseases[J]. Antioxidants (Basel), 2021, 10:1939.doi:10.3390/antiox10121939.
[12]	Dakroub A, Suzanne AN, Firas Kobeissy, et al. Visfatin:An emerging adipocytokine bridging the gap in the evolution of cardiovascular diseases[J]. J Cell Physiol, 2021, 236:6282-6296.
[13]	Bossardi Ramos R, Adam AP. Molecular mechanisms of vascular damage during lung injury[J]. Adv Exp Med Biol, 2021, 1304:95-107.
[14]	Olszańska J, Pietraszek-Gremplewicz K, Nowak D. Melanoma progression under obesity:focus on adipokines[J]. Cancers (Basel), 2021, 13:2281.doi:10.3390/cancers13092281.
[15]	Bermudez T,Sammani S, Hernon VR, et al. eNAMPT neutralization reduces preclinical ARDS severity via rectified NFκB and Akt/mTORC2 signaling[J].Sci Rep, 2022, 12:696.doi:10.1038/s41598-021-04444-9.
[16]	Song J, Deng T. The Adipocyte and Adaptive Immunity[J]. Front Immunol, 2020, 11:593058.doi:10.3389/fimmu.2020.593058.
[17]	Audrito V, Messana VG, Deaglio S. NAMPT and NAPRT: two metabolic enzymes with key roles in inflammation[J]. Front Oncol, 2020, 10:358.doi:10.3389/fonc.2020.00358.eCollection2020.
[18]	Karampela I, Christodoulatos GS, Kandri E, et al. Circulating eNampt and resistin as a proinflammatory duet predicting independently mortality in critically ill patients with sepsis:a prospective observational study[J]. Cytokine, 2019, 119:62-70.
[19]	Koch A, Weiskirchen R, Krusch A, et al. Visfatin serum levels predict mortality in critically Ⅲ patients[J]. Dis Markers, 2018, 2018:7315356.doi:10.1155/2018/7315356.eCollection2018.
[20]	Meyer NJ, Gattinoni L, Calfee CS. Acute respiratory distress syndrome[J]. Lancet, 2021, 398:622-637.
[21]	Bime C, Casanova N, Oita RC, et al. Development of a biomarker mortality risk model in acute respiratory distress syndrome[J]. Crit Care, 2019, 23:410.doi:10.1186/s13054-019-2697-x.
[22]	Quijada H, Bermudez T, Kempf CL, et al. Endothelial eNAMPT amplifies pre-clinical acute lung injury:efficacy of an eNAMPT-neutralising monoclonal antibody[J]. Eur Respir J, 2021, 57:2002536.doi:10.1183/13993003.02536-2020.Print 2021 May.
[23]	Liu L, Wang P, Liang C, et al. Distinct effects of Nampt inhibition on mild and severe models of lipopolysaccharide-induced myocardial impairment[J]. Int Immunopharmacol, 2013, 17:342-349.
[24]	李文蕾,霍洪亮. Visfatin对心肌细胞炎性因子ICAM-1,VCAM-1表达的影响[D].长春,东北师范大学, 2011, 11:1-40.
[25]	Heo YJ, Choi SE, Lee N, et al. Visfatin exacerbates hepatic inflammation and fibrosis in a methionine-choline-deficient diet mouse model[J]. J Gastroenterol Hepatol, 2021, 36:2592-2600.
[26]	Moschen AR, Gerner R, Schroll A, et al. A key role for Pre-B cell colony-enhancing factor in experimental hepatitis[J]. Hepatology, 2011, 54:675-686.

内脂素在脓毒症相关性脏器损伤中的作用及机制研究进展

Research progress on the role and mechanism of visfatin in sepsis-related organ injury

PDF

可视化

摘要/Abstract

引用本文

使用本文

参考文献 26

相关文章 13

编辑推荐

Metrics

本文评价

[1]	孙晓丽, 张进进, 宋凤英, 黄永莉, 陈立力, 邢颜超. Tim-3/galectin-9调控脂多糖诱导的人淋巴细胞中Th1/Th2细胞平衡[J]. 基础医学与临床, 2023, 43(10): 1542-1548.
[2]	王英臣, 孙立群. 二肽基肽酶Ⅲ在治疗脓毒症中的应用进展[J]. 基础医学与临床, 2023, 43(1): 196-199.
[3]	薛晋芳, 宋海飞, 陈国兵. 程序性细胞死亡在脓毒症发生发展中的研究进展[J]. 基础医学与临床, 2022, 42(8): 1284-1287.
[4]	林柏柏, 钱风华, 钱义明, 赵雷, 孙旗, 褚梦瑶, 沈梦雯. 脓毒症并发毛细血管渗漏综合征的研究进展[J]. 基础医学与临床, 2022, 42(7): 1144-1147.
[5]	温燕, 林金灿, 黄颖泓, 肖文彪, 张民伟, 林建东. 脓毒症早期BMP-2和BMP-4的变化[J]. 基础医学与临床, 2022, 42(4): 628-632.
[6]	石丹丹, 蒋素芳, 王茜, 赵鹏博, 刘雅. IL-6反式信号传导通路抑制剂sgp130Fc抑制脓毒症小鼠炎性反应及调节免疫细胞[J]. 基础医学与临床, 2022, 42(12): 1895-1899.
[7]	李嘉晋, 刘军, 何松于, 谌浩云. 下调miR-27a减轻脓毒症模型大鼠肺损伤[J]. 基础医学与临床, 2022, 42(11): 1704-1708.
[8]	王玉龙, 滕文彬, 单跃, 姚刘旭, 何锐, 李玉红, 祝胜美. HIF-1α激动剂或拮抗剂对脓毒症大鼠肠道黏膜通透性的影响[J]. 基础医学与临床, 2021, 41(11): 1618-1623.
[9]	邵瑞飞, 杨艳, 郑志榕, 赵世民, 陈国兵. 肠道菌群和“肠-肺”轴在脓毒症中的作用[J]. 基础医学与临床, 2020, 40(8): 1109-1112.
[10]	何锐, 朱烨柯, 滕文彬, 单跃, 易声华, 祝胜美, 李玉红. 甘油可能通过水通道蛋白3减轻脓毒症小鼠肠黏膜屏障损伤[J]. 基础医学与临床, 2020, 40(5): 655-661.
[11]	文大林, 杜娟, 陈民佳, 孙剑会, 张华才, 张安强, 都定元. 联合检测C反应蛋白和降钙素原在创伤后脓毒症患者早期预警中的作用[J]. 基础医学与临床, 2020, 40(2): 178-181.
[12]	吴铭蒋苇苇高莉莉. 脂氧素A4降低LPS致肥胖大鼠炎性因子的释放[J]. 基础医学与临床, 2018, 38(12): 1749-1752.
[13]	王瑞兰魏乔康福新曹戍李国平茹松伟李彩花. 眼镜蛇毒因子抑制脓毒症大鼠的炎症反应[J]. 基础医学与临床, 2008, 28(11): 1178-1182.