Endothelial dysfunction, arterial stiffness and vascular inflammation in hypertension

Hypertension is increasingly recognized not just as elevated blood pressure, but as a systemic vascular disease. At the heart of its pathophysiology lies a detrimental triad: endothelial dysfunction, arterial stiffness, and chronic vascular inflammation. Endothelial dysfunction often serves as an initial trigger, representing a functional impairment of the vascular lining that compromises its ability to regulate vascular tone and maintain an anti-inflammatory surface. This functional impairment promotes a pro-inflammatory environment within the vessel wall. Concurrently, structural changes lead to increased arterial stiffness, a loss of vascular compliance that is an active pathological process elevating systolic pressure and cardiovascular risk. These three components are not isolated but are deeply intertwined, creating a self-reinforcing cycle where dysfunction fuels inflammation, which in turn drives stiffness, further impairing endothelial health. This integrated framework is fundamental to the progression of hypertension from a hemodynamic disorder to a multisystem disease affecting the heart, brain, and kidneys. A holistic understanding of this interplay is crucial for developing new therapeutic strategies.

This Research Topic aims to create a comprehensive forum exploring the complex interrelationships between endothelial dysfunction, arterial stiffness, and vascular inflammation in hypertension pathophysiology. Despite significant advances in understanding these individual components, their integrated roles in hypertension development and progression remain incompletely characterized. We seek to compile cutting-edge research illuminating novel molecular mechanisms, signaling pathways, and cellular interactions that link these three pathophysiological processes. The Research Topic will highlight emerging biomarkers for early detection, innovative therapeutic targets, and translational approaches that address this pathological triad. By bringing together basic science investigations, clinical studies, and therapeutic innovations, we endeavor to foster a multidisciplinary perspective that advances both our fundamental understanding of hypertension pathophysiology and the development of more effective, mechanism-based interventions to improve patient outcomes in this prevalent cardiovascular condition.

● Molecular and cellular mechanisms connecting endothelial dysfunction, arterial stiffness, and inflammation in hypertension, with emphasis on specific signaling pathways and mediators

● Novel biomarkers and diagnostic approaches for early detection and monitoring of endothelial dysfunction, arterial stiffness, and vascular inflammation in hypertensive patients

● Advanced imaging techniques and functional assessments for quantifying vascular changes in hypertension, including flow-mediated dilation, pulse wave velocity, and inflammatory imaging

● Pharmacological and non-pharmacological interventions specifically targeting the endothelial-arterial stiffness-inflammation axis in hypertension management

● Sex-specific, age-related, and ethnic differences in the manifestation and progression of endothelial dysfunction, arterial stiffness, and vascular inflammation in hypertension

● Clinical implications and risk stratification based on combined assessment of endothelial function, arterial stiffness, and inflammatory markers in primary and secondary hypertension
• Mechanisms of atherosclerosis in the context of hypertension.
• Vascular imaging and biomarkers of atherosclerotic disease.
• Therapeutic interventions targeting both atherosclerosis and hypertension.
• Clinical and translational studies on cardiovascular risk stratification.