Extracellular matrix: paving the way to the newest trends in atherosclerosis

Purpose of review The extracellular matrix (ECM) is critical for all aspects of vascular pathobiology. In vascular disease the balance of its structural components is shifted. In atherosclerotic plaques there is in fact a dynamic battle between stabilizing and proinflammatory responses. This review explores the most recent strides that have been made to detail the active role of the ECM - and its main binding partners - in driving atherosclerotic plaque development and destabilization. Recent findings Proteoglycans-glycosaminoglycans (PGs-GAGs) synthesis and remodelling, as well as elastin synthesis, cross-linking, degradation and its elastokines potentially affect disease progression, providing multiple steps for potential therapeutic intervention and diagnostic targeted imaging. Of note, GAGs biosynthetic enzymes modulate the phenotype of vascular resident and infiltrating cells. In addition, while plaque collagen structure exerts very palpable effects on its immediate surroundings, a new role for collagen is also emerging on a more systemic level as a biomarker for cardiovascular disease as well as a target for selective drug-delivery. The importance of studying the ECM in atherosclerosis is more and more acknowledged and various systems are being developed to visualize, target and mimic it.

Automated summary

Recent studies have highlighted the critical role of ECM and its main binding partners in driving the development and destabilization of atherosclerotic plaques. Key findings include the impact of PGs-GAGs synthesis, elastin synthesis, and plaque collagen structure on disease progression, offering potential therapeutic interventions and diagnostic imaging targets. The growing acknowledgment of the importance of studying the ECM in atherosclerosis has led to the development of various systems to visualize, target, and mimic its functions.