Red blood cells actively contribute to endothelial dysfunction and atherosclerosis by leading to decreased vascular resilience and stability.
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This paper provides a systems-dynamic interpretation of recent findings suggesting that red blood cells may actively contribute to endothelial dysfunction and atherosclerosis. Rather than viewing atherosclerosis solely as a lipid-driven or inflammatory process, the analysis frames disease development as a gradual loss of vascular resilience leading to a critical transition. Using the Universal Resonance Model (URM) as a conceptual framework, the paper interprets erythrocyte–endothelium interactions as manifestations of declining system stability, characterized by increased variability, delayed recovery, and reduced adaptive capacity. From this perspective, atherosclerosis emerges as a dynamic process rather than a linear accumulation of damage. The work does not present new experimental data but offers a theoretical synthesis intended to connect molecular observations with broader system-level behavior. It highlights how stabilizing interventions applied during pre-critical phases may have disproportionate clinical impact and suggests a role for resilience-based approaches in cardiovascular prevention. NoteThis work represents a conceptual and interpretive contribution. It does not present new experimental or clinical data but offers a systems-dynamic perspective on previously reported findings. The interpretation is intended to support interdisciplinary dialogue and to situate vascular pathology within a broader framework of biological resilience and disease emergence.
Anita Domargård (Sun,) reported a other. Red blood cells actively contribute to endothelial dysfunction and atherosclerosis by leading to decreased vascular resilience and stability.
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