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<p>A hallmark of myocardial ischemia/reperfusion (I/R) injury is the dysregulated apoptosis of neutrophils, which constitutes a key pathogenic driver. The primary aim of this research was to determine the regulatory influence of Krüppel-like factor 2 (KLF2) on neutrophil apoptosis and to clarify the implicated signaling pathways within the setting of myocardial I/R injury. To establish myocardial I/R injury, C57BL/6J mice underwent surgical occlusion of the left anterior descending coronary artery. Bone marrow-derived neutrophils (BMDNs) were isolated, with purity and apoptosis assessed by flow cytometry. KLF2 expression was genetically modulated (overexpression/knockdown) in neutrophils, followed by Notch pathway inhibition using DAPT. qRT-PCR and Western blot quantified KLF2, Notch1, Bax, Bcl-2, and cleaved-caspase3 expression. Myocardial injury was quantified via TTC staining, H&amp;E staining, and Masson staining. KLF2 overexpression markedly enhanced neutrophil apoptosis, concurrent with Notch1 activation, elevated Bax and cleaved-caspase3, and suppressed Bcl-2. Pharmacological inhibition of Notch signaling using DAPT reversed KLF2-driven apoptosis. In vivo, I/R induced myocardial damage, manifested as extensive myocardial infarction, inflammatory infiltration, and collagen deposition. However, these detrimental effects were ameliorated after overexpression of KLF2. KLF2 promotes neutrophil apoptosis during I/R injury by upregulating Notch1 expression, thereby highlighting its promise as a novel therapeutic intervention for myocardial I/R injury.</p>

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KLF2 Promotes Neutrophil Apoptosis in Mice with Myocardial ischemia-reperfusion Injury by Upregulating Notch1

  • 期刊论文

  • 发表日期：

    2025年9月12日

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  • Furu Nie,
  • Xu Deng

摘要

A hallmark of myocardial ischemia/reperfusion (I/R) injury is the dysregulated apoptosis of neutrophils, which constitutes a key pathogenic driver. The primary aim of this research was to determine the regulatory influence of Krüppel-like factor 2 (KLF2) on neutrophil apoptosis and to clarify the implicated signaling pathways within the setting of myocardial I/R injury. To establish myocardial I/R injury, C57BL/6J mice underwent surgical occlusion of the left anterior descending coronary artery. Bone marrow-derived neutrophils (BMDNs) were isolated, with purity and apoptosis assessed by flow cytometry. KLF2 expression was genetically modulated (overexpression/knockdown) in neutrophils, followed by Notch pathway inhibition using DAPT. qRT-PCR and Western blot quantified KLF2, Notch1, Bax, Bcl-2, and cleaved-caspase3 expression. Myocardial injury was quantified via TTC staining, H&E staining, and Masson staining. KLF2 overexpression markedly enhanced neutrophil apoptosis, concurrent with Notch1 activation, elevated Bax and cleaved-caspase3, and suppressed Bcl-2. Pharmacological inhibition of Notch signaling using DAPT reversed KLF2-driven apoptosis. In vivo, I/R induced myocardial damage, manifested as extensive myocardial infarction, inflammatory infiltration, and collagen deposition. However, these detrimental effects were ameliorated after overexpression of KLF2. KLF2 promotes neutrophil apoptosis during I/R injury by upregulating Notch1 expression, thereby highlighting its promise as a novel therapeutic intervention for myocardial I/R injury.