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中华临床医师杂志(电子版) ›› 2025, Vol. 19 ›› Issue (08) : 612 -617. doi: 10.3877/cma.j.issn.1674-0785.2025.08.009

综述

5-羟色胺与铁死亡介导的脓毒症心肌病的研究进展
周懿1, 黄容华1, 刘政疆1,2,()   
  1. 1 533000 广西百色,右江民族医学院研究生院
    2 533000 广西百色,右江民族医学院附属医院心血管内科
  • 收稿日期:2025-07-07 出版日期:2025-08-30
  • 通信作者: 刘政疆
  • 基金资助:
    2024年度广西壮族自治区卫生健康委自筹经费科研课题(Z-L20240820)

Research progress of 5-hydroxytryptamine and ferroptosis-mediated septic cardiomyopathy

Yi Zhou1, Ronghua Huang1, Zhengjiang Liu1,2,()   

  1. 1 Graduate School of Youjiang Medical University for Nationalities, Baise 533000, China
    2 Department of Cardiovascular Medicine, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, China
  • Received:2025-07-07 Published:2025-08-30
  • Corresponding author: Zhengjiang Liu
引用本文:

周懿, 黄容华, 刘政疆. 5-羟色胺与铁死亡介导的脓毒症心肌病的研究进展[J/OL]. 中华临床医师杂志(电子版), 2025, 19(08): 612-617.

Yi Zhou, Ronghua Huang, Zhengjiang Liu. Research progress of 5-hydroxytryptamine and ferroptosis-mediated septic cardiomyopathy[J/OL]. Chinese Journal of Clinicians(Electronic Edition), 2025, 19(08): 612-617.

脓毒症可引发多系统并发症,其中心肌损伤是最常见的严重并发症之一,也是脓毒症患者预后不良的重要标志。铁死亡作为新近发现的程序性细胞死亡方式,已被证实参与脓毒症心肌病的发生发展过程。5-羟色胺作为炎症介质,虽已被证明可促进脓毒症进展,但其通过铁死亡途径介导心脏损伤的具体机制尚未完全明确。本文对5-HT在SCM中的作用机制进行总结,旨在为临床治疗提供新的干预靶点和策略。

Sepsis can lead to multiple systemic complications, with myocardial injury being one of the most frequent and severe complications, and serving as a crucial prognostic marker in septic patients. Ferroptosis, a recently identified form of programmed cell death, has been shown to participate in the pathogenesis of septic cardiomyopathy (SCM). As an inflammatory mediator, 5-hydroxytryptamine (5-HT) has been demonstrated to promote sepsis progression, yet its precise mechanism in mediating cardiac injury via ferroptosis remains incompletely understood. This review systematically summarizes the mechanistic role of 5-HT in SCM, aiming to provide novel therapeutic targets and clinical strategies.

图1 5-HT与铁死亡介导的脓毒症心肌病的关系简图 注:5-HT为5-羟色胺;5-HTR为5-羟色胺受体
图2 5-HT与铁死亡介导的脓毒症心肌病的机制图 注:箭头表示促进作用,平头表示抑制作用。CLP为盲肠结扎穿刺术;5-HT3R为5-HT3受体;sST2为可溶性生长刺激表达基因2蛋白,是白细胞介素-1受体家族的重要成员;CK-MB为肌酸激酶同工酶MB;Cardiomyocyte为心肌细胞;Tropisetron为托烷司琼;5-HT2BR为5-HT2B受体;PI3K为磷脂酰肌醇-3-激酶;Akt又称PKB,为蛋白激酶B;mTOR为哺乳动物雷帕霉素靶蛋白;HIF1α为缺氧诱导因子-1α;ABCD1为ATP结合盒转运蛋白D亚家族成员1;5-HT为5-羟色胺;Fyn为酪氨酸蛋白激酶Fyn;MAO-A为单胺氧化酶A;ROS为活性氧;NF-κB为核因子κB;SSRIs为选择性5-羟色胺再摄取抑制剂;SERT为5-羟色胺再摄取转运蛋白;Glutamate为谷氨酸;Cystine为胱氨酸;SLC3A2为溶质载体家族3成员2;SLC7A11为溶质载体家族7成员11;Cysteine为半胱氨酸;GSH为谷胱甘肽;Se为硒;GPX4为谷胱甘肽过氧化酶4;Lipid peroxides为脂质过氧化物;Ferroptosis为铁死亡;PUFAs为多不饱和脂肪酸;ACSL4为乙酰辅酶A合成酶长链家族成员4;LPCAT3为溶血磷脂酰胆碱酰基转移酶3;PUFAs-PE为多不饱和脂肪酸磷脂;LOX为脂氧合酶;POR为细胞色素P450氧化还原酶;PUFAs-OOH为脂质过氧化氢;PUFAs-OH为脂质醇;GTP为鸟苷三磷酸;GCH1为GTP环化水解酶1;BH4为四氢生物蝶呤;BH2即7,8-dihydrobiopterin,为7,8-二氢生物蝶呤;DHFR为二氢叶酸还原酶;CoQH2为泛醇;CoQ10为泛醌;FSP1为铁死亡抑制蛋白1;LPS为脂多糖;SLC39A14为溶质载体家族39成员14;LIP为不稳定铁池;Fenton为芬顿反应;Tf为转铁蛋白;TfR1为转铁蛋白受体1;Endosome为内体;STEAP3为STEAP3金属还原酶;Ferritin为铁蛋白;NCOA4为核受体共激活因子4;Ferritinophagy为铁自噬;SFXN1为线粒体膜蛋白sideroflexin1;DHODH为二氢乳清酸脱氢酶;mGPX4为线粒体GPX4;Mitochondrion为线粒体;5-HT1AR为5-HT1A受体;Immune cells为免疫细胞
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