Key result
Stress hyperglycemia impairs post-MI cardiac repair by driving FOXK2 degradation in macrophages.
Stress hyperglycemia impairs macrophage-mediated cardiac repair after myocardial infarction by promoting O-GlcNAcylation and ubiquitin-proteasome-dependent degradation of FOXK2.
FOXK2 reduction in SHG may impair post-MI macrophage repair; leaves open therapeutic targeting pending validation.
Stress hyperglycemia (SHG) predicts poor outcomes after myocardial infarction (MI), but the underlying mechanisms remain unclear. Here, we identify FOXK2 as a key regulator of macrophage-mediated cardiac repair. FOXK2 expression was reduced in cardiac macrophages from hyperglycemic mice after MI and in peripheral blood mononuclear cells from patients with MI with SHG, whereas macrophage-specific FOXK2 deficiency aggravated cardiac injury. Under high-glucose conditions, FOXK2 was glycosylated at T552 by O-GlcNAc transferase, promoting its ubiquitin-proteasome-dependent degradation. Mass spectrometry and functional assays showed that the FOXK2
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Lv et al. (2026) studied Myocardial infarction with stress hyperglycemia. Stress hyperglycemia / macrophage-specific FOXK2 deficiency was evaluated on Macrophage-mediated cardiac repair and cardiac injury after myocardial infarction. Stress hyperglycemia impairs macrophage cardiac repair post-MI by promoting O-GlcNAcylation of FOXK2 at T552 and its ubiquitin-proteasome degradation.
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