急性心肌梗死后血管生成的调控及其治疗应用
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(海军军医大学附属长海医院心内科,上海市 200433)

作者简介:

努尔柯孜·阿卜杜合力力,硕士研究生,研究方向为冠状动脉粥样硬化性心脏病,E-mail:3445775378@qq.com。

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基金项目:

国家自然科学基金项目(81760076、82070419)


Regulation of angiogenesis after acute myocardial infarction and its therapeutic applications
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Department of Cardiology, Changhai Hospital, Naval Military Medical University, Shanghai 200433, China)

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    摘要:

    急性心肌梗死仍然是死亡率较高的心血管疾病,促进梗死后的血管生成可以促进血运重建、改善心肌功能,其对于心肌损伤后的修复具有重要意义。心肌梗死后的血管生成从梗死边界区开始并延伸到坏死的梗死核心,血管生成过程较复杂,其机制尚未完全阐明;有多个信号传导通路可调控血管生成的过程,包括磷脂酰肌醇3激酶/蛋白激酶B(PI3K/Akt)通路、Notch(Notch)信号通路、Janus激酶/信号转导与转录激活因子(JAK/STAT)通路以及刺猬信号通路(Shh)等。阐明心肌梗死后血管生成的相关信号通路机制,可为心肌梗死后的血管生成治疗提供研究方向和证据。文章对心肌梗死后血管生成特点及各信号传导通路在血管生成中的相关机制作一综述。

    Abstract:

    Acute myocardial infarction is still a cardiovascular disease with high mortality. Promoting angiogenesis after infarction can promote revascularization and improve myocardial function, which is of great significance for the repair of myocardial injury. Angiogenesis after myocardial infarction starts from the infarct boundary area and extends to the necrotic infarction core, the process of angiogenesis is complex, and its mechanisms have not been fully elucidated; there are several signal transduction pathways that can regulate the process of angiogenesis, including phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), Notch signaling pathway (Notch), janus kinase/signal transducer and activator of transcription (JAK/STAT) and sonic hedgehog signaling pathway (Shh), etc. Elucidating the related mechanisms of angiogenesis after myocardial infarction through various signal transduction pathways can provide research evidence and direction for the treatment of angiogenesis after myocardial infarction. This article reviews the characteristics of angiogenesis after myocardial infarction and the related mechanisms of signal transduction pathways in angiogenesis.

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努尔柯孜·阿卜杜合力力,吴弘.急性心肌梗死后血管生成的调控及其治疗应用[J].中国动脉硬化杂志,2025,33(12):1083~1091.

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  • 收稿日期:2024-06-16
  • 最后修改日期:2025-07-13
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  • 在线发布日期: 2025-12-30