• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

脓毒症中心肌细胞死亡:机制与调控(综述)。

Cardiomyocyte death in sepsis: Mechanisms and regulation (Review).

机构信息

Department of Critical Care Medicine, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, P.R. China.

出版信息

Mol Med Rep. 2022 Aug;26(2). doi: 10.3892/mmr.2022.12773. Epub 2022 Jun 15.

DOI:10.3892/mmr.2022.12773
PMID:35703348
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9218731/
Abstract

Sepsis‑induced cardiac dysfunction is one of the most common types of organ dysfunction in sepsis; its pathogenesis is highly complex and not yet fully understood. Cardiomyocytes serve a key role in the pathophysiology of cardiac function; due to the limited ability of cardiomyocytes to regenerate, their loss contributes to decreased cardiac function. The activation of inflammatory signalling pathways affects cardiomyocyte function and modes of cardiomyocyte death in sepsis. Prevention of cardiomyocyte death is an important therapeutic strategy for sepsis‑induced cardiac dysfunction. Thus, understanding the signalling pathways that activate cardiomyocyte death and cross‑regulation between death modes are key to finding therapeutic targets. The present review focused on advances in understanding of sepsis‑induced cardiomyocyte death pathways, including apoptosis, necroptosis, mitochondria‑mediated necrosis, pyroptosis, ferroptosis and autophagy. The present review summarizes the effect of inflammatory activation on cardiomyocyte death mechanisms, the diversity of regulatory mechanisms and cross‑regulation between death modes and the effect on cardiac function in sepsis to provide a theoretical basis for treatment of sepsis‑induced cardiac dysfunction.

摘要

脓毒症相关性心功能障碍是脓毒症中最常见的器官功能障碍类型之一;其发病机制非常复杂,尚未完全阐明。心肌细胞在心脏功能的病理生理学中起着关键作用;由于心肌细胞的再生能力有限,其丧失导致心功能下降。炎症信号通路的激活影响脓毒症中心肌细胞的功能和死亡方式。预防心肌细胞死亡是脓毒症相关性心功能障碍的重要治疗策略。因此,了解激活心肌细胞死亡的信号通路以及死亡方式之间的交叉调控是寻找治疗靶点的关键。本综述重点介绍了对脓毒症诱导的心肌细胞死亡途径的理解进展,包括细胞凋亡、坏死性凋亡、线粒体介导的坏死、细胞焦亡、铁死亡和自噬。本综述总结了炎症激活对心肌细胞死亡机制、调控机制多样性以及死亡方式之间交叉调控的影响以及对脓毒症中心脏功能的影响,为脓毒症相关性心功能障碍的治疗提供理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8904/9218731/75d3737a51c2/mmr-26-02-12773-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8904/9218731/75d3737a51c2/mmr-26-02-12773-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8904/9218731/75d3737a51c2/mmr-26-02-12773-g00.jpg

相似文献

1
Cardiomyocyte death in sepsis: Mechanisms and regulation (Review).脓毒症中心肌细胞死亡:机制与调控(综述)。
Mol Med Rep. 2022 Aug;26(2). doi: 10.3892/mmr.2022.12773. Epub 2022 Jun 15.
2
Minocycline promotes cardiomyocyte mitochondrial autophagy and cardiomyocyte autophagy to prevent sepsis-induced cardiac dysfunction by Akt/mTOR signaling.米诺环素通过 Akt/mTOR 信号通路促进心肌细胞线粒体自噬和心肌细胞自噬,预防脓毒症引起的心脏功能障碍。
Apoptosis. 2019 Apr;24(3-4):369-381. doi: 10.1007/s10495-019-01521-3.
3
Sepsis‑induced cardiac dysfunction and pathogenetic mechanisms (Review).脓毒症相关性心功能障碍及其发病机制的研究进展(综述)。
Mol Med Rep. 2023 Dec;28(6). doi: 10.3892/mmr.2023.13114. Epub 2023 Oct 20.
4
PINK1 contained in huMSC-derived exosomes prevents cardiomyocyte mitochondrial calcium overload in sepsis via recovery of mitochondrial Ca efflux.人骨髓间充质干细胞来源的外泌体中含有的 PINK1 通过恢复线粒体钙外流来防止脓毒症中心肌细胞线粒体钙超载。
Stem Cell Res Ther. 2021 May 6;12(1):269. doi: 10.1186/s13287-021-02325-6.
5
Alox15/15-HpETE Aggravates Myocardial Ischemia-Reperfusion Injury by Promoting Cardiomyocyte Ferroptosis.Alox15/15-HpETE 通过促进心肌细胞铁死亡加重心肌缺血再灌注损伤。
Circulation. 2023 May 9;147(19):1444-1460. doi: 10.1161/CIRCULATIONAHA.122.060257. Epub 2023 Mar 29.
6
Hyperoside prevents sepsis-associated cardiac dysfunction through regulating cardiomyocyte viability and inflammation via inhibiting miR-21.金丝桃苷通过抑制 miR-21 调节心肌细胞活力和炎症来预防脓毒症相关性心功能障碍。
Biomed Pharmacother. 2021 Jun;138:111524. doi: 10.1016/j.biopha.2021.111524. Epub 2021 Apr 1.
7
Fundamental Mechanisms of Regulated Cell Death and Implications for Heart Disease.调控细胞死亡的基本机制及其对心脏病的影响。
Physiol Rev. 2019 Oct 1;99(4):1765-1817. doi: 10.1152/physrev.00022.2018.
8
Overview of pyroptosis mechanism and in-depth analysis of cardiomyocyte pyroptosis mediated by NF-κB pathway in heart failure.细胞焦亡机制概述及 NF-κB 通路介导心力衰竭中心肌细胞焦亡的深入分析。
Biomed Pharmacother. 2024 Oct;179:117367. doi: 10.1016/j.biopha.2024.117367. Epub 2024 Aug 29.
9
Regulated cell death pathways in doxorubicin-induced cardiotoxicity.多柔比星诱导心脏毒性中的调控细胞死亡途径。
Cell Death Dis. 2021 Apr 1;12(4):339. doi: 10.1038/s41419-021-03614-x.
10
SP1-induced ZFAS1 aggravates sepsis-induced cardiac dysfunction via miR-590-3p/NLRP3-mediated autophagy and pyroptosis.SP1 诱导的 ZFAS1 通过 miR-590-3p/NLRP3 介导的自噬和焦亡加重脓毒症诱导的心脏功能障碍。
Arch Biochem Biophys. 2020 Nov 30;695:108611. doi: 10.1016/j.abb.2020.108611. Epub 2020 Sep 29.

引用本文的文献

1
Roles and Therapeutic Targeting of Exosomes in Sepsis-Induced Cardiomyopathy.外泌体在脓毒症诱导的心肌病中的作用及治疗靶点
J Cell Mol Med. 2025 Apr;29(8):e70559. doi: 10.1111/jcmm.70559.
2
Fermented Juice Exerts Cardioprotective Effects by Alleviating Cardiac Inflammation and Apoptosis in Rats with Lipopolysaccharide-Induced Sepsis.发酵果汁通过减轻脂多糖诱导的脓毒症大鼠的心脏炎症和细胞凋亡发挥心脏保护作用。
Nutrients. 2025 Jan 29;17(3):501. doi: 10.3390/nu17030501.
3
Levosimendan for sepsis-induced myocardial dysfunction: friend or foe?

本文引用的文献

1
Receptor Interacting Protein Kinases 1/3: The Potential Therapeutic Target for Cardiovascular Inflammatory Diseases.受体相互作用蛋白激酶1/3:心血管炎性疾病的潜在治疗靶点。
Front Pharmacol. 2021 Nov 18;12:762334. doi: 10.3389/fphar.2021.762334. eCollection 2021.
2
Potent and Selective RIPK1 Inhibitors Targeting Dual-Pockets for the Treatment of Systemic Inflammatory Response Syndrome and Sepsis.强效且选择性的 RIPK1 抑制剂靶向双口袋结构,用于治疗全身炎症反应综合征和脓毒症。
Angew Chem Int Ed Engl. 2022 Jan 26;61(5):e202114922. doi: 10.1002/anie.202114922. Epub 2021 Dec 16.
3
RIPK1 and TRADD Regulate TNF-Induced Signaling and Ripoptosome Formation.
左西孟旦治疗脓毒症诱发的心肌功能障碍:是福是祸?
Front Cardiovasc Med. 2025 Jan 8;11:1520596. doi: 10.3389/fcvm.2024.1520596. eCollection 2024.
4
Dexmedetomidine regulates exosomal miR-29b-3p from macrophages and alleviates septic myocardial injury by promoting autophagy in cardiomyocytes via targeting glycogen synthase kinase 3β.右美托咪定调节巨噬细胞来源的外泌体 miR-29b-3p,并通过靶向糖原合酶激酶 3β 促进心肌细胞自噬来减轻脓毒症心肌损伤。
Burns Trauma. 2024 Nov 4;12:tkae042. doi: 10.1093/burnst/tkae042. eCollection 2024.
5
Septic Cardiomyopathy.脓毒症性心肌病
Rev Cardiovasc Med. 2024 Jan 15;25(1):23. doi: 10.31083/j.rcm2501023. eCollection 2024 Jan.
6
PTX3 mediates PI3K/AKT/mTOR signaling to downregulate apoptosis and autophagy to attenuate myocardial injury in sepsis.PTX3 通过介导 PI3K/AKT/mTOR 信号通路下调细胞凋亡和自噬从而减轻脓毒症心肌损伤。
PeerJ. 2024 May 20;12:e17263. doi: 10.7717/peerj.17263. eCollection 2024.
7
N6-Methyladenosine Demethylase ALKBH5 Promotes Pyroptosis by Modulating PTBP1 mRNA Stability in LPS-Induced Myocardial Dysfunction.N6-甲基腺苷去甲基化酶ALKBH5通过调节PTBP1 mRNA稳定性促进脂多糖诱导的心肌功能障碍中的细胞焦亡。
Acta Cardiol Sin. 2024 May;40(3):312-321. doi: 10.6515/ACS.202405_40(3).20240127A.
8
Phospholipid transfer protein ameliorates sepsis-induced cardiac dysfunction through NLRP3 inflammasome inhibition.磷脂转运蛋白通过抑制NLRP3炎性小体改善脓毒症诱导的心脏功能障碍。
Open Med (Wars). 2024 Mar 27;19(1):20240915. doi: 10.1515/med-2024-0915. eCollection 2024.
9
Molecular hydrogen attenuates sepsis-induced cardiomyopathy in mice by promoting autophagy.分子氢通过促进自噬减轻小鼠脓毒症诱导的心肌病。
BMC Anesthesiol. 2024 Feb 23;24(1):72. doi: 10.1186/s12871-024-02462-4.
10
Klotho activation of Nrf2 inhibits the ferroptosis signaling pathway to ameliorate sepsis-associated acute kidney injury.Klotho激活Nrf2可抑制铁死亡信号通路,以改善脓毒症相关的急性肾损伤。
Transl Androl Urol. 2023 Dec 31;12(12):1871-1884. doi: 10.21037/tau-23-573. Epub 2023 Dec 21.
RIPK1 和 TRADD 调节 TNF 诱导的信号转导和 Ripoptosome 形成。
Int J Mol Sci. 2021 Nov 18;22(22):12459. doi: 10.3390/ijms222212459.
4
The Link Between Ferroptosis and Cardiovascular Diseases: A Novel Target for Treatment.铁死亡与心血管疾病之间的联系:一种新的治疗靶点。
Front Cardiovasc Med. 2021 Jul 22;8:710963. doi: 10.3389/fcvm.2021.710963. eCollection 2021.
5
Inflammation and Cell Death of the Innate and Adaptive Immune System during Sepsis.脓毒症时固有免疫和适应性免疫系统的炎症和细胞死亡。
Biomolecules. 2021 Jul 10;11(7):1011. doi: 10.3390/biom11071011.
6
Pretreatment of cardiac progenitor cells with bradykinin attenuates HO-induced cell apoptosis and improves cardiac function in rats by regulating autophagy.预处理心脏祖细胞用缓激肽可通过调节自噬减轻 HO 诱导的细胞凋亡,改善大鼠心功能。
Stem Cell Res Ther. 2021 Aug 5;12(1):437. doi: 10.1186/s13287-021-02503-6.
7
Ferroptosis: a cell death connecting oxidative stress, inflammation and cardiovascular diseases.铁死亡:一种连接氧化应激、炎症与心血管疾病的细胞死亡方式。
Cell Death Discov. 2021 Jul 26;7(1):193. doi: 10.1038/s41420-021-00579-w.
8
PINK1 contained in huMSC-derived exosomes prevents cardiomyocyte mitochondrial calcium overload in sepsis via recovery of mitochondrial Ca efflux.人骨髓间充质干细胞来源的外泌体中含有的 PINK1 通过恢复线粒体钙外流来防止脓毒症中心肌细胞线粒体钙超载。
Stem Cell Res Ther. 2021 May 6;12(1):269. doi: 10.1186/s13287-021-02325-6.
9
Targeting Ferroptosis against Ischemia/Reperfusion Cardiac Injury.靶向铁死亡治疗缺血/再灌注心脏损伤
Antioxidants (Basel). 2021 Apr 25;10(5):667. doi: 10.3390/antiox10050667.
10
Ferroptotic cell death triggered by conjugated linolenic acids is mediated by ACSL1.共轭亚油酸触发的铁死亡细胞死亡是由 ACSL1 介导的。
Nat Commun. 2021 Apr 14;12(1):2244. doi: 10.1038/s41467-021-22471-y.