Advanced Glycation End Products and Psoriasis

Abstract

Advanced glycation end products (AGEs) are biologically active compounds formed physiologically throughout a sequence of chemical reactions, to generate highly oxidant-reactive aldehydes that combine covalently to proteins. They accumulate slowly in tissues during ageing but also in metabolic and selected inflammatory disorders. Accumulation of AGEs occurs more rapidly and intensely in the skin and serum of patients with type 2 diabetes, obesity, cardiovascular diseases, chronic renal insufficiency, and non-alcoholic fatty liver disease and also in the skin of patients with psoriasis. All of the above conditions are intimately associated with psoriasis. Interaction of AGEs with their receptors (RAGEs) stimulates cellular signaling with the formation of reactive oxygen species and activation of nuclear factor kappa light chain enhancer of activated B (NF-kB), which is a key regulator in the expression of inflammatory mediators and the production of oxidative stress. Thus, AGEs may play an interesting pathogenic role in the intersection of inflammatory and metabolic diseases, may represent a biomarker of inflammation and a potential target for novel therapeutic strategies. This is a narrative review with the objective to summarize current evidence on the role of AGEs in psoriasis.

Effects of tumor necrosis factor-alpha inhibitors on lipid profiles in patients with psoriasis: a systematic review and meta-analysis

“…Psoriasis is characterized by the formation of silvery-white scaly plaques, and its adverse effect on emotionally and physically relevant quality of life is comparable to other major diseases ( 1 , 3 ). Of note, psoriasis is a typical inflammatory skin disease whose pathogenesis usually involves the activation of inflammatory processes that have the potential to influence systemic organ responses and functions, which in turn results in the dysfunction of various organs ( 4 – 6 ). Indeed, increasing clinical observations have converged to evidence the high prevalence of co-morbidities in patients with psoriasis ( 7 , 8 ).…”

Metabolic dysfunction associated steatotic liver disease in patients with plaque psoriasis: a case–control study and serological comparison

“…Furthermore, the metabolic complications associated with psoriasis have gained significant attention, increasingly viewed as an immunometabolic disorder ( 15 ). Key metabolic pathways such as glycolysis, the tricarboxylic acid cycle, lipid metabolism, and amino acid metabolism are vital in regulating keratinocytes and immune cells ( 16 , 17 ). The link between psoriasis and metabolic complications may stem from a common genetic basis, chronic inflammation, immune regulation, and oxidative stress ( 18 ).…”