慢性心力衰竭的炎性机制研究进展
摘要
<正>随着社会变迁及人文环境的变化,慢性心力衰竭(CHF)的发病率逐年提高,其病程长、病情迁延、再住院率及病死率均很高,已严重威胁着人类的健康。CHF受心室重构、神经内分泌、体液因子及炎性细胞因子等多种机制的调控,且各机制之间相互影响,共同成为调节CHF的机制网。其中炎性反应与心力衰竭密切相关。炎性细胞因子是由免疫系统细胞产生的内源性肽,具有生物学效应,可介导多种免疫应答。炎性细胞因子与心力衰竭的发生发展密切相关。心力衰竭时,因受多种因素的刺
引文
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[8] Teng X,Hu Z,Wei X,et al. IL-37 ameliorates the inflammatory process in psoriasis by suppressing proinflammatory cytokine production[J]. J Immunol,2014,192(4):1815-1823. DOI:10. 4049/jimmunol. 1300047.
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[11] Shukat K,Jennifer J,Marqulies KB,et al. Enhancedbioactive myocardial transforming growth factor-βin advanced human heart failure[J]. Circulation,2014,78(11):2711-2718.
[12] Wen H,Miao EA,Ting JP. Mechanisms of NOD-like receptor-Associated inflammasome activation[J]. Immunity,2013,39(3):432-441. DOI:10. 1016/j. immuni. 2013. 08. 037.
[13]舒成霖,何燕. NLRP3炎症小体对心力衰竭后心律失常的影响[J].中国循环杂志,2016,10(31):1025-1027. DOI:10. 3969/j. issn. 1000-3614. 2016. 10. 018.
[14]曾春雨.诱导多能干细胞和心脏干/祖细胞对心肌修复作用的研究进展[J].解放军医药杂志,2012,24(7):1-4. DOI:10.3969/j. issn. 2095-140X. 2012. 07. 001.
[15]刘兆杰,杨娟,李文茜.慢性心力衰竭相关的炎性因子的探讨[J].心血管病学进展,2018,39(3):388-391. DOI:10. 16806/j. cnki. issn. 1004-3934. 2018. 03. 021.
[2] Mac Gowan GA,Mann DL,Kormos PL,et al. Circu lating interleukin-6in severe heart failure[J]. Am J Cardiol,1997,79(8):1128-1131.
[3]邓新桃,郑金国,石桂良,等. IL-6及BNP与心力衰竭的关系[J].南京医科大学学报(自然科学版). 2014,10(34):1350-1351.DOI:10. 7655/NYDXBNS20141013.
[4] Sonderegger I,Rhn TA,Kurrer MO,et al. Neutralization of IL-17 by active vaccination inhibits IL-23-dependent autoimmune myocarditis[J]. European journal of immunology. 2006. 36(11):2849-2856.DOI:10. 1002/eji. 200636484.
[5]刘冉.心力衰竭患者血清IL-17及IL-35水平的变化及其临床意义[D].苏州:苏州大学,2014.
[6]陈宝峰,徐新.白细胞介素-18与动脉粥样硬化危险因素的相关性[J].中国心血管杂志,2008,13(6):456-458.
[7] Sets Y,Kanda T,Tanaka T,et al. Interleukin-18 in patients with congestive heart failure:induction of atrial natriuretic peptide gene expression[J]. Res Commun Mol Pathol Pharmacol,2000,108(1-2):87-95.
[8] Teng X,Hu Z,Wei X,et al. IL-37 ameliorates the inflammatory process in psoriasis by suppressing proinflammatory cytokine production[J]. J Immunol,2014,192(4):1815-1823. DOI:10. 4049/jimmunol. 1300047.
[9]齐杰.脑内氧化应激参与心力衰竭时交感神经兴奋的研究[D].太原:山西医科大学,2012.
[10] Eisen A,Benderly M,Behar S,et al. Inflammation and future risk of symptomatic heart failure in patients with stable coronary artery disease[J]. Am Heart J. 2014,167(5):707-714. DOI:10. 1016/j.ahj. 2014. 01. 008.
[11] Shukat K,Jennifer J,Marqulies KB,et al. Enhancedbioactive myocardial transforming growth factor-βin advanced human heart failure[J]. Circulation,2014,78(11):2711-2718.
[12] Wen H,Miao EA,Ting JP. Mechanisms of NOD-like receptor-Associated inflammasome activation[J]. Immunity,2013,39(3):432-441. DOI:10. 1016/j. immuni. 2013. 08. 037.
[13]舒成霖,何燕. NLRP3炎症小体对心力衰竭后心律失常的影响[J].中国循环杂志,2016,10(31):1025-1027. DOI:10. 3969/j. issn. 1000-3614. 2016. 10. 018.
[14]曾春雨.诱导多能干细胞和心脏干/祖细胞对心肌修复作用的研究进展[J].解放军医药杂志,2012,24(7):1-4. DOI:10.3969/j. issn. 2095-140X. 2012. 07. 001.
[15]刘兆杰,杨娟,李文茜.慢性心力衰竭相关的炎性因子的探讨[J].心血管病学进展,2018,39(3):388-391. DOI:10. 16806/j. cnki. issn. 1004-3934. 2018. 03. 021.