PDF(Pubmed)
Abstract：
Aging leads to physiological changes, including inflammaging-a chronic low-grade inflammatory state with significant implications for various physiological systems, particularly for cardiovascular health. Concurrently, immunosenescence-the age-related decline in immune function, exacerbates vulnerabilities to cardiovascular pathologies in older individuals. Examining the dynamic connections between immunosenescence, inflammation, and cardiovascular aging, this mini-review aims to disentangle some of these interactions for a better understanding of their complex interplay. In the context of cardiovascular aging, the chronic inflammatory state associated with inflammaging compromises vascular integrity and function, contributing to atherosclerosis, endothelial dysfunction, arterial stiffening, and hypertension. The aging immune system\'s decline amplifies oxidative stress, fostering an environment conducive to atherosclerotic plaque formation. Noteworthy inflammatory markers, such as the high-sensitivity C-reactive protein, interleukin-6, interleukin-1β, interleukin-18, and tumor necrosis factor-alpha emerge as key players in cardiovascular aging, triggering inflammatory signaling pathways and intensifying inflammaging and immunosenescence. In this review we aim to explore the molecular and cellular mechanisms underlying inflammaging and immunosenescence, shedding light on their nuanced contributions to cardiovascular diseases. Furthermore, we explore the reciprocal relationship between immunosenescence and inflammaging, revealing a self-reinforcing cycle that intensifies cardiovascular risks. This understanding opens avenues for potential therapeutic targets to break this cycle and mitigate cardiovascular dysfunction in aging individuals. Furthermore, we address the implications of Long COVID, introducing an additional layer of complexity to the relationship between aging, immunosenescence, inflammaging, and cardiovascular health. Our review aims to stimulate continued exploration and advance our understanding within the realm of aging and cardiovascular health.
摘要：
衰老导致生理变化，包括炎症-一种对各种生理系统有重大影响的慢性低度炎症状态，特别是对于心血管健康。同时,免疫衰老-与年龄相关的免疫功能下降，加剧老年人心血管疾病的脆弱性。检查免疫衰老之间的动态联系，炎症,和心血管老化，这篇小型评论旨在解开这些相互作用中的一些，以便更好地理解它们复杂的相互作用。在心血管衰老的背景下，与炎症相关的慢性炎症状态会损害血管的完整性和功能，导致动脉粥样硬化，内皮功能障碍,动脉硬化,和高血压。衰老的免疫系统的衰退放大了氧化应激，培养有利于动脉粥样硬化斑块形成的环境。值得注意的炎症标志物，比如高敏C反应蛋白,白细胞介素-6，白细胞介素-1β，白细胞介素-18和肿瘤坏死因子-α成为心血管衰老的关键参与者，触发炎症信号通路并加剧炎症和免疫衰老。在这篇综述中，我们旨在探讨炎症和免疫衰老的分子和细胞机制。揭示了他们对心血管疾病的微妙贡献。此外，我们探讨了免疫衰老和炎症之间的相互关系，揭示了一个自我强化的循环，加剧了心血管风险。这种理解为潜在的治疗目标开辟了途径，以打破这种循环并减轻衰老个体的心血管功能障碍。此外，我们讨论了长COVID的影响，为衰老之间的关系引入了额外的复杂性，免疫衰老，发炎，和心血管健康。我们的审查旨在促进持续的探索，并促进我们对衰老和心血管健康领域的理解。
