From biomimicry to clinical actionability: rethinking high-shear thrombosis as a mechanobiological system
Marcus Vinicius Batista da Silva, Christopher A. Bresette, Viviana ClaveríaPurpose of review
Arterial thrombosis remains a leading cause of morbidity and mortality worldwide, while its mechanistic understanding and clinical management remain limited. In this review, we discuss how recent advances in microfluidic thrombosis models, mechanobiology, and microrobotic technologies may enable the development of clinically actionable and personalized thrombosis platforms.
Recent findings
Recent findings demonstrate that arterial thrombus formation is strongly regulated by dynamic shear stress, platelet-rich aggregation, and von Willebrand factor (vWF)-mediated interactions. Emerging evidence further shows that shear-induced platelet aggregates, also known as SIPA clots, can form mechanically robust thrombi independently of classical coagulation pathways, highlighting thrombosis as a highly mechanosensitive process. Although microfluidic and flow-based systems have improved the physiological modeling of thrombosis, current platforms still face major limitations in capturing multidimensional shear dynamics, mechanobiological complexity, and patient-specific variability.
Summary
Recent progress in vessel-on-a-chip technologies, computational modeling, artificial intelligence, and microrobotic systems suggests a pathway toward integrated and feedback-driven thrombosis management. These approaches may enable not only the measurement and prediction of thrombotic behavior but also its active modulation through targeted interventions. Collectively, this perspective supports a transition from static thrombosis assays toward dynamic and controllable mechanobiological platforms for precision cardiovascular medicine.