Abnormal inflammatory traits and downregulated caveolin-1 expression in monocytes of psoriasis patients may be associated with psoriatic inflammation and atherosclerosis

Crosstalk between cholesterol metabolism and psoriatic inflammation

“…Another study also showed that serum total cholesterol, and triglyceride in the high-fat-feed rats decreased after being injected with the IL-17 neutralizing antibody ( 126 ). LDL peroxidation results in oxidized low-density lipoprotein, often known as “ oxidized low-density lipoprotein (ox-LDL).” Ox-LDL is taken up by transmembrane scavenger receptors like SR-B1 and CD36, as well as by the lectin-like oxidized LDL receptor-1 (LOX-1) ( 127 , 128 ). Excess oxygen metabolites overwhelm the antioxidant capacity of the organism, which is one of the important features of psoriasis ( 129 ).…”

“…also found that ox-LDL boosted IL-23 expression in TNF-α stimulated KCs via LOX-1, which is elevated and linked with the severity of the disease in psoriatic patients ( 127 , 132 ). On the other hand, by over-expressing CD36 to uptake ox-LDL and form foam cells, psoriatic monocytes are more likely to evolve into M1 pro-inflammatory macrophages that produce psoriatic cytokines and raise the risk of cardiovascular disease comorbidity ( 128 ). In turn, pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6, which are increased in psoriasis, can activate LOX-1, promoting the uptake of ox-LDL by macrophages ( 133 ).…”

Caveolin-1 in endothelial cells: A potential therapeutic target for atherosclerosis

“…Similarly, Cav1 has been reported negatively regulate inflammation, and its overexpression inhibits silica-induced inflammatory cell infiltration and reduces inflammatory factor release. Cav1 −/− mouse models exhibit severe silicosis injury and fibrosis, and Cav1 expression is downregulated in LPS-induced acute lung injury due to specific mechanisms involving TLR4-NF-κB inflammatory signaling pathway inhibition and reduced cellular oxidative stress and macrophage M1 differentiation [ [133] , [134] , [135] , [136] ].…”

Involvement of caveolin-1 in skin diseases

“…Decreased CAV-1 expression in monocytes was reversed when patients were treated with anti-TNF-α antibodies, suggesting that psoriasis-related inflammatory cytokines also reduce CAV-1 expression in monocytes ( 15 ). Moreover, circulating monocytes in patients with psoriasis are innately polarized to the M1 phenotype, which contributes to the development of atherosclerosis ( 86 ). Silencing of CAV-1 expression in healthy monocytes prompts the polarization of macrophages to the M1 phenotype and might increase the risk of atherosclerosis by increasing macrophage oxidized low-density lipoprotein uptake ( 86 ).…”

“…Moreover, circulating monocytes in patients with psoriasis are innately polarized to the M1 phenotype, which contributes to the development of atherosclerosis ( 86 ). Silencing of CAV-1 expression in healthy monocytes prompts the polarization of macrophages to the M1 phenotype and might increase the risk of atherosclerosis by increasing macrophage oxidized low-density lipoprotein uptake ( 86 ). Leptin, an adipocyte-derived hormone, is correlated with obesity and psoriasis severity ( 87 , 88 ).…”