ArticleCell biochemistry and biophysics2026
KLF2 Promotes Neutrophil Apoptosis in Mice with Myocardial ischemia-reperfusion Injury by Upregulating Notch1.
Article in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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