Queiroz Marcelo, Sena Cristina M
Institute of Physiology, iCBR, Faculty of Medicine, University of Coimbra, Subunit 1, polo 3, Azinhaga de Santa Comba, Celas, 3000-548, Coimbra, Portugal.
Cardiovasc Diabetol. 2024 Dec 28;23(1):455. doi: 10.1186/s12933-024-02549-9.
Perivascular adipose tissue (PVAT) is a dynamic tissue that affects vascular function and cardiovascular health. The connection between PVAT, the immune system, obesity, and vascular disease is complex and plays a pivotal role in the pathogenesis of vascular diseases such as atherosclerosis, hypertension, and vascular inflammation. In cardiometabolic diseases, PVAT becomes a significant source of proflammatory adipokines, leading to increased infiltration of immune cells, in cardiometabolic diseases, PVAT becomes a significant source of proinflammatory adipokines, leading to increased infiltration of immune cells, promoting vascular smooth muscle cell proliferation and migrationpromoting vascular smooth muscle cell proliferation and migration. This exacerbates vascular dysfunction by impairing endothelial cell function and promoting endothelial activation. Dysregulated PVAT also contributes to hemodynamic alterations and hypertension through enhanced sympathetic nervous system activity and impaired vasodilatory capacity of PVAT-derived factors. Therapeutic interventions targeting key components of this interaction, such as modulating PVAT inflammation, restoring adipokine balance, and attenuating immune cell activation, hold promise for mitigating obesity-related vascular complications. Lifestyle interventions, pharmacological agents targeting inflammatory pathways, and surgical approaches aimed at reducing PVAT mass or improving adipose tissue function are potential therapeutic avenues for managing vascular diseases associated with obesity and PVAT dysfunction.
血管周围脂肪组织(PVAT)是一种影响血管功能和心血管健康的动态组织。PVAT、免疫系统、肥胖与血管疾病之间的联系错综复杂,在动脉粥样硬化、高血压和血管炎症等血管疾病的发病机制中起着关键作用。在心脏代谢疾病中,PVAT成为促炎脂肪因子的重要来源,导致免疫细胞浸润增加,促进血管平滑肌细胞增殖和迁移,通过损害内皮细胞功能和促进内皮激活加剧血管功能障碍。PVAT失调还通过增强交感神经系统活动和损害PVAT衍生因子的血管舒张能力导致血流动力学改变和高血压。针对这种相互作用的关键成分进行治疗干预,如调节PVAT炎症、恢复脂肪因子平衡和减弱免疫细胞激活,有望减轻肥胖相关的血管并发症。生活方式干预、针对炎症途径的药物以及旨在减少PVAT质量或改善脂肪组织功能的手术方法是管理与肥胖和PVAT功能障碍相关的血管疾病的潜在治疗途径。