Fig. 7
From: Contribution of TLR4 signaling in intermittent hypoxia-mediated atherosclerosis progression
Possible mechanism diagram of IH accelerated atherosclerotic plaque growth and instability. IH exposure enhanced the expression of TLR4 and facilitated the activation of NF-κB p65 both in vivo and in vitro. Activated NF-κB entered the nucleus and augmented the expression of inflammatory cytokines. Inflammatory activity accelerated atherosclerotic plaque growth and instability. In summary, IH promotes atherosclerosis progression mainly through activating inflammatory response, which depends on TLR4/NF-κB signaling