Endothelial dysfunction is a central feature of cardiovascular disease (CVD) and reflects the maladaptive integration of hemodynamic, metabolic, and inflammatory cues within the vascular microenvironment. The endothelial Notch signaling pathway has emerged as a conserved regulatory pathway whose output is highly dependent on cellular context. While its developmental roles are well established, how endothelial Notch integrates mechanical, inflammatory, and metabolic cues in adult CVD remains incompletely defined. Addressing this gap is essential for understanding why both excessive and insufficient Notch activation are associated with cardiovascular pathology. This review synthesizes current evidence defining the mechanistic regulation of endothelial Notch signaling and contextualizes its dysregulation across major CVD phenotypes, highlighting the need for precision-based therapeutic strategies that restore physiological Notch signaling without global pathway suppression.
Campbell et al. (Sat,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: