Apolipoprotein (a)/Lipoprotein(a)-Induced Oxidative-Inflammatory <i>α</i>7-nAChR/p38 MAPK/IL-6/RhoA-GTP Signaling Axis and M1 Macrophage Polarization Modulate Inflammation-Associated Development of Coronary Artery Spasm

<div>Graphical abstract depicting how Lp(a)-triggered inflammation drives CAS through macrophage M1 polarization, activation of coronary VSMC, and <i>α</i>7-nAChR/p38 MAPK signal induction. Tocilizumab disrupts Lp(a)-induced <i>α</i>7-nAChR/p38 signaling by attenuating the inflammation in coronary VSMCs and patient monocyte-derived macrophages.</div>

Oxidative Medicine and Cellular Longevity

fig6

Figure 6

Figure 6: Apolipoprotein (a)/Lipoprotein(a)-Induced Oxidative-Inflammatory <i>α</i>7-nAChR/p38 MAPK/IL-6/RhoA-GTP Signaling Axis and M1 Macrophage Polarization Modulate Inflammation-Associated Development of Coronary Artery Spasm 

Figure 6 | Apolipoprotein (a)/Lipoprotein(a)-Induced Oxidative-Inflammatory α7-nAChR/p38 MAPK/IL-6/RhoA-GTP Signaling Axis and M1 Macrophage Polarization Modulate Inflammation-Associated Development of Coronary Artery Spasm 