Life sciences · 2026
Sfrp5 protects acute myocardial infarction by inhibiting macrophage foam cell formation and apoptosis via modulation of macrophage polarization and p38-MAPK/JNK/NF-κB pathways.
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Du Xia-Xia, Shuai Shi-Feng, Wang Ting, Zhang Jia-Nan, Liu Zhao-Hui, Sun Yu-Qi, Zhou Li-Zhen, Li Ji-Shen, Wang Kai, Tong Shan
Аннотация
AIMS: To investigate the role of secreted frizzled-related protein 5 (Sfrp5) in ST-segment elevation myocardial infarction (STEMI) and its protective mechanisms in macrophage-driven plaque instability.
MATERIALS AND METHODS: Serum Sfrp5 levels were measured in 89 STEMI and 65 stable angina pectoris (SAP) patients. Foam macrophage models were established using murine RAW264.7 and human THP-1-derived macrophages. Sfrp5 effects on foam cell formation, apoptosis, and M1/M2 polarization were assessed, along with p38-MAPK/JNK/NF-κB signaling modulation using specific activators/inhibitors and RNA sequencing.
KEY FINDINGS: STEMI patients showed significantly lower serum Sfrp5 levels (P < 0.0001), negatively correlated with peak troponin T (P = 0.013). Sfrp5 suppressed foam cell formation, apoptosis, and M1 polarization while promoting M2 polarization in vitro. Inhibition of M2 polarization attenuated these effects. Mechanistically, Sfrp5 exerted protection by suppressing the p38-MAPK/JNK/NF-κB signaling axis, confirmed by RNA sequencing showing altered expression of genes involved in lipid metabolism, inflammation, and apoptosis.
SIGNIFICANCE: Sfrp5 enhances atherosclerotic plaque stability by inhibiting macrophage foam cell formation and apoptosis via suppression of p38-MAPK/JNK/NF-κB signaling and modulation of macrophage polarization, representing a potential therapeutic target for STEMI.
MATERIALS AND METHODS: Serum Sfrp5 levels were measured in 89 STEMI and 65 stable angina pectoris (SAP) patients. Foam macrophage models were established using murine RAW264.7 and human THP-1-derived macrophages. Sfrp5 effects on foam cell formation, apoptosis, and M1/M2 polarization were assessed, along with p38-MAPK/JNK/NF-κB signaling modulation using specific activators/inhibitors and RNA sequencing.
KEY FINDINGS: STEMI patients showed significantly lower serum Sfrp5 levels (P < 0.0001), negatively correlated with peak troponin T (P = 0.013). Sfrp5 suppressed foam cell formation, apoptosis, and M1 polarization while promoting M2 polarization in vitro. Inhibition of M2 polarization attenuated these effects. Mechanistically, Sfrp5 exerted protection by suppressing the p38-MAPK/JNK/NF-κB signaling axis, confirmed by RNA sequencing showing altered expression of genes involved in lipid metabolism, inflammation, and apoptosis.
SIGNIFICANCE: Sfrp5 enhances atherosclerotic plaque stability by inhibiting macrophage foam cell formation and apoptosis via suppression of p38-MAPK/JNK/NF-κB signaling and modulation of macrophage polarization, representing a potential therapeutic target for STEMI.
Предметные рубрики MeSH
HumansAnimalsApoptosisNF-kappa BFoam CellsMicep38 Mitogen-Activated Protein KinasesMacrophagesMaleSecreted Frizzled-Related ProteinsMyocardial InfarctionRAW 264.7 CellsSignal TransductionFemaleMiddle AgedAdaptor Proteins, Signal TransducingMembrane ProteinsTHP-1 CellsST Elevation Myocardial InfarctionPlaque, AtheroscleroticMAP Kinase Signaling System