Misfolded plasma protein signature in carotid artery dissection

Abstract Carotid artery dissection (CAD) is a leading cause of ischaemic stroke in young adults, yet its underlying molecular mechanisms remain insufficiently understood. Disruptions in cellular protein homeostasis and accumulation of misfolded proteins may play a key role in the structural weakening of the arterial wall. In this study, we used a surface plasmon resonance (SPR) biosensor combined with the Heat shock protein 70 (Hsp70) trap assay and tandem mass spectrometry (LC-MS/MS) to detect and characterise misfolded proteins in the plasma of patients with CAD. We analysed samples from 21 CAD patients and 21 healthy controls and revealed 38 proteins with significant quantitative differences between the two groups. These proteins are involved in cell adhesion, coagulation, inflammation, and lipid metabolism—processes relevant to vascular integrity and CAD pathogenesis. A panel of five selected proteins demonstrated strong discriminatory power between CAD patients and controls. Our findings support the hypothesis that disturbances in proteostasis and related molecular pathways contribute to the pathophysiology of CAD. The identified proteomic signature may serve as a promising source of serum biomarkers for the early identification of individuals at increased risk of carotid artery dissection.