Neuro-immune-vascular interactions in rosacea and hypertension: a mechanistic review

Rosacea is a chronic inflammatory skin disorder characterized by recurrent flare-ups and significant variability in therapeutic responses. Its pathophysiology is complex and involves multilevel processes, including neurogenic dysregulation, immune activation, and alterations in vascular reactivity. Recent epidemiological studies suggest that rosacea may be associated with an increased risk of hypertension and other cardiometabolic diseases. However, it remains unclear whether this association merely reflects a comorbidity or indicates the presence of shared underlying pathophysiological mechanisms. Therefore, from an integrated neuro-immune-vascular perspective, this review summarizes current evidence regarding potential shared neuro-immune-vascular mechanisms that may be associated with rosacea and hypertension. Emerging evidence suggests that aberrant activation of sensory nerves, neuropeptide release, and subsequent innate and adaptive immune responses may collectively participate in a putative regulatory network. Locally, this network may be associated with neurogenic inflammation and aberrant vasodilation in the skin; at the systemic level, it may potentially be associated with dysregulated blood pressure control through mechanisms such as chronic low-grade inflammation, endothelial dysfunction, and vascular remodeling. By synthesizing evidence from dermatology, immunology, and vascular biology, this review summarizes potential neuro-immune-vascular interactions associated with rosacea and hypertension and discusses their possible implications for comorbidity management.