Fig. 1

Progression and Classification of Vascular Remodeling. A When a stimulus is applied to an artery, stress factors (shear stress and circumferential wall stress) deviate from their normal steady state. The artery compensates for this perturbation by changing the vessel diameter through relaxation or contraction. If the stimulus is short-term, the change in vessel diameter is also temporary. B Conversely, if pro-hypertensive stimuli persists for a prolonged period, vascular component cells exhibit dramatic changes in transcription profiles, including ion channels that regulate intracellular Ca²⁺ signaling. This can result in electrical remodeling causing enhanced vasocontractility. At the same time, vasodilator capacity and endothelial barrier integrity are impaired. These changes cause functional remodeling. In addition, macrophages traffic to, and accumulate in the adventitia of blood vessels where they promote structural remodeling that enhances arterial stiffness and changes vessel diameter. In combination, these functional and structural remodeling lead to chronic hypertension. C Structural remodeling is classified on the basis of changes in vessel diameter and cross-sectional area. In hypertension, outward hypertrophic remodeling is observed in elastic arteries, whereas inward eutrophic remodeling or inward hypertrophic remodeling is observed in resistance arteries. In atherosclerosis, outward hypertrophic remodeling is observed in large vessels. EDHF: endothelium-derived hyperpolarizing factor, EGF: epidermal growth factor, ET-1: endothelin-1, NAd: noradrenaline