Cytokines play a crucial role in the structure and function of blood vessels in hypertension. Hypertension damages blood vessels by mechanisms linked to shear forces, activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, oxidative stress, and a proinflammatory milieu that lead to the generation of neoantigens and damage-associated molecular patterns, ultimately triggering the release of numerous cytokines. Damage-associated molecular patterns are recognized by PRRs (pattern recognition receptors) and activate inflammatory mechanisms in endothelial cells, smooth muscle cells, perivascular nerves, and perivascular adipose tissue. Activated vascular cells also release cytokines and express factors that attract macrophages, dendritic cells, and lymphocytes to the blood vessels. Activated and differentiated T cells into Th1, Th17, and Th22 in secondary lymphoid organs migrate to the vessels, releasing specific cytokines that further contribute to vascular dysfunction and remodeling. This chronic inflammation alters the profile of endothelial and smooth muscle cells, making them dysfunctional. Here, we provide an overview of how cytokines contribute to hypertension by impacting the vasculature. Furthermore, we explore clinical perspectives about the modulation of cytokines as a potential therapeutic intervention to specifically target hypertension-linked vascular dysfunction.

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细胞因子在高血压中的免疫调节活性：血管视角

细胞因子在高血压血管的结构和功能中起着至关重要的作用。高血压通过与剪切力、肾素-血管紧张素-醛固酮和交感神经系统的激活、氧化应激以及促炎环境相关的机制损害血管，这些机制导致新抗原的产生和损伤相关的分子模式，最终触发释放许多细胞因子。损伤相关分子模式被 PRR（模式识别受体）识别，并激活内皮细胞、平滑肌细胞、血管周围神经和血管周围脂肪组织中的炎症机制。活化的血管细胞还释放细胞因子并表达吸引巨噬细胞、树突状细胞和淋巴细胞到血管的因子。次级淋巴器官中活化并分化为 Th1、Th17 和 Th22 的 T 细胞迁移至血管，释放特定细胞因子，进一步导致血管功能障碍和重塑。这种慢性炎症改变内皮细胞和平滑肌细胞的形态，使它们功能失调。在这里，我们概述了细胞因子如何通过影响脉管系统而导致高血压。此外，我们探讨了细胞因子调节作为一种潜在的治疗干预措施的临床观点，以专门针对高血压相关的血管功能障碍。