ArticleTranslational stroke research2025
Long-Term Course of Circulating Elastin, Collagen Type I, and Collagen Type III in Patients with Spontaneous Cervical Artery Dissection: a Prospective Multicenter Study.
Article in Translational stroke research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Risk factors for cervical artery dissection: a systematic review with meta-analysis.Stroke and vascular neurology · 2026Pooled it
- Targeting CX3CR1 Signaling Dynamics: A Critical Determinant in the Temporal Regulation of Post-Stroke Neurorepair.Brain sciences · 2025Review
- Elevated serum levels of anti-collagen type I antibodies in patients with spontaneous cervical artery dissection and ischemic stroke: a prospective multicenter study.Frontiers in immunology · 2024Article
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Authors and funding
7 authors.
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Abstract
An impaired integrity of vascular elements and the extracellular matrix (ECM) has been discussed to play a critical role in the pathophysiology of spontaneous cervical artery dissection (sCAD). This study aimed to explore the temporal course of circulating elastin, collagen type I, and collagen type III in patients with sCAD and evaluated their eligibility as diagnostic biomarkers. Patients with sCAD were prospectively enrolled in four German stroke centers. Blood samples were collected at baseline (acute phase), at day 10 ± 3 (subacute phase), and after 6 ± 1 months (chronic phase). Patients with acute ischemic stroke not related to sCAD, healthy probands, and patients undergoing thromboendarterectomy of the carotid artery served as control groups. Serum levels of elastin and collagen types I and III were determined by ELISAs. Fifty-seven patients with sCAD were enrolled. Compared to all three control groups, patients with sCAD had significantly lower levels of elastin and collagen type III at baseline and after 6 months. Compared to healthy probands, patients with sCAD showed similar collagen type I levels at baseline and in the subacute phase, but significantly increased levels after 6 months. As serum levels of elastin, collagen types I and III were not elevated in the acute phase, they do not appear eligible as biomarkers for the diagnosis of sCAD. Persisting low serum levels of elastin and collagen type III towards the chronic phase of sCAD strengthens the hypothesis of a subtle, in most cases clinically inapparent affection of the ECM in patients with sCAD.
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