Protective Effects of Hydroxychloroquine against Accelerated Atherosclerosis in Systemic Lupus Erythematosus

Table 1

Possible protective effects of HCQ on the interplay between atherosclerosis and SLE pathogenesis.

Features of SLE pathogenesis	HCQ	Features of atherosclerosis pathogenesis
Imbalance between endothelial damage and repair mechanisms		Endothelial dysfunction
Increased oxidative stress		Endothelial damage and impaired vasodilatation
Increased macrophage activation		Monocyte recruitment and activation in atherosclerotic plaques
Hyperactive T-cell with increased survival		T-cell recruitment and activation in atherosclerotic plaques
Dysregulation of TLR2 and TLR4 activation; activation of TLR7 and TLR9 by anti-DNA		Overexpression and activation of TLRs (especially TLR2/TLR4)
Increased levels of IFNα		Increased activation of macrophages and foam cells in the atherosclerotic plaques
Increased levels of TNF-α, IL-17, IL-6		Increased macrophage activation, adhesion molecule expression, chemotaxis, and inhibition of SMC proliferation
Increased levels of IFN-γ		Increased expression of adhesion molecule expression and inhibition of SMC proliferation and collagen production
Increased prevalence of anti-ApoA-1 antibodies and proinflammatory HDL		Decreased antiatherosclerosis HDL function

The arrows represent the interplay between SLE and atherogenesis. The crosses represent the proved (black) or potential (blank) action of HCQ in inhibiting the proatherogenic effect of SLE.