Department of Structural and Functional Biology, Institute of Biosciences, UNESP - São Paulo State University, Zip Code: 510, P.O Box: 18618-689, Botucatu, São Paulo, Brazil.
Universidad Maimónides, Ciudad Autónoma de Buenos Aires, Argentina.
Curr Hypertens Rep. 2022 Nov;24(11):547-562. doi: 10.1007/s11906-022-01214-4. Epub 2022 Jul 7.
This review summarizes the involvement of inflammaging in vascular damage with focus on the epigenetic mechanisms by which inflammaging-induced hypertension is triggered.
Inflammaging in hypertension is a complex condition associated with the production of inflammatory mediators by the immune cells, enhancement of oxidative stress, and tissue remodeling in vascular smooth muscle cells and endothelial cells. Cellular processes are numerous, including inflammasome assembly and cell senescence which may involve mitochondrial dysfunction, autophagy, DNA damage response, dysbiosis, and many others. More recently, a series of noncoding RNAs, mainly microRNAs, have been described as possessing epigenetic actions on the regulation of inflammasome-related hypertension, emerging as a promising therapeutic strategy. Although there are a variety of pharmacological agents that effectively regulate inflammaging-related hypertension, a deeper understanding of the epigenetic events behind the control of vessel deterioration is needed for the treatment or even to prevent the disease onset.
本篇综述总结了炎症与血管损伤的关系,并重点介绍了炎症引起高血压的表观遗传机制。
高血压中的炎症衰老与免疫细胞产生炎症介质、氧化应激增强以及血管平滑肌细胞和内皮细胞的组织重塑有关。细胞过程很多,包括炎症小体的组装和细胞衰老,这可能涉及线粒体功能障碍、自噬、DNA 损伤反应、菌群失调和许多其他因素。最近,一系列非编码 RNA,主要是 microRNAs,被描述为对炎症小体相关高血压具有表观遗传作用,这为治疗提供了一种很有前景的策略。尽管有多种药物可有效调节与炎症相关的高血压,但为了治疗甚至预防疾病的发生,还需要深入了解控制血管恶化的表观遗传事件。