Asprosin as a Potential Biomarker for Disease Activity in Behcet Disease

Behçet's disease (BD) is a chronic, recurrent, multisystem inflammatory vasculitis characterized by various systemic manifestations involving all vessel sizes in both the arterial and venous systems [1,2].

Given that BD is a prototypical systemic vasculitis in which endothelial damage and vascular inflammation are central pathogenic mechanisms, the identification of novel biomarkers reflecting vascular involvement is of major clinical importance[3].

Asprosin is an adipokine that beyond its metabolic effects, carries growing evidence suggesting its associated with vascular pathologies [4].

Experimental and clinical studies have demonstrated that Asprosin contributes to endothelial dysfunction, induces phenotypic switching in vascular smooth muscle cells, and facilitates vascular remodeling by activating pro-inflammatory signaling pathways such as TLR4-NF-κB-NLRP3 [4,5]. Furthermore, Asprosin has been implicated in endothelial-to-mesenchymal transition through TGF-β signaling, thereby exacerbating peripheral arterial disease and vascular stiffness[4,5]. Although endothelial dysfunction and surrogate markers of vascular injury (e.g., impaired flow-mediated dilation, increased intima-media thickness, oxidative stress markers) have been extensively studied in BD[3], the role of Asprosin in this disease remains unexplored.

In this context, Asprosin may represent a link between metabolic pathways and immune mediated vascular inflammation, warranting investigation in systemic vasculitis as potential biomarkers of disease activity [6].