Current Hypertension Reports ( IF 3.9 ) Pub Date : 2022-07-07 , DOI: 10.1007/s11906-022-01214-4
Vinícius Augusto Simão 1 , León Ferder 2 , Walter Manucha 3, 4 , Luiz Gustavo A Chuffa 1
Purpose of Review
This review summarizes the involvement of inflammaging in vascular damage with focus on the epigenetic mechanisms by which inflammaging-induced hypertension is triggered.
Recent Findings
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.
Summary
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.
中文翻译:
炎症相关高血压的表观遗传机制
审查目的
这篇综述总结了炎症在血管损伤中的作用,重点是引发炎症性高血压的表观遗传机制。
最近的发现
高血压炎症是一种复杂的疾病,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,包括炎性体组装和细胞衰老,这可能涉及线粒体功能障碍、自噬、DNA 损伤反应、生态失调等。最近,一系列非编码 RNA,主要是 microRNA,被描述为具有调节炎性体相关高血压的表观遗传作用,成为一种有前途的治疗策略。
概括
尽管有多种药物可以有效调节与炎症相关的高血压,但治疗甚至预防疾病发作需要更深入地了解控制血管恶化背后的表观遗传事件。