Chiriacò Martina, Georgiopoulos Georgios, Duranti Emiliano, Antonioli Luca, Puxeddu Ilaria, Nannipieri Monica, Rosada Javier, Blandizzi Corrado, Taddei Stefano, Virdis Agostino, Masi Stefano
Department of Clinical and Experimental Medicine, Università di Pisa, Santa Chiara Hospital, Via Roma, 67, 56126, Pisa, Italy.
First Department of Cardiology, Hippokration Hospital, University of Athens, Athens, Greece.
High Blood Press Cardiovasc Prev. 2019 Aug;26(4):321-329. doi: 10.1007/s40292-019-00331-7. Epub 2019 Jul 19.
Cardiovascular disease (CVD) remains the leading cause of morbility and mortality worldwide. The identification of common cardiovascular risk factors has led to the development of effective treatments that enabled a significant reduction of the global cardiovascular disease burden. However, a significant proportion of cardiovascular risk remains unexplained by these risk factors leaving many individuals at risk of cardiovascular events despite good control of the risk factors. Recent randomized clinical trials and Mendelian randomization studies have suggested that inflammation explains a significant proportion of the residual cardiovascular risk in subjects with good control of risk factors. An accelerated process of vascular ageing is increasingly recognized as a potential mechanism by which inflammation might increase the risk of CVD. In turn, cellular ageing represents an important source of inflammation within the vascular wall, potentially creating a vicious cycle that might promote progression of atherosclerosis, independently from the individual cardiovascular risk factor burden. In this review, we summarise current evidence suggesting a role for biological ageing in CVD and how inflammation might act as a key mediator of this association.
心血管疾病（CVD）仍然是全球发病和死亡的主要原因。常见心血管危险因素的识别促使了有效治疗方法的发展，从而显著降低了全球心血管疾病负担。然而，这些危险因素仍无法解释很大一部分心血管风险，这使得许多人尽管对危险因素进行了良好控制，但仍有发生心血管事件的风险。最近的随机临床试验和孟德尔随机化研究表明，炎症在危险因素得到良好控制的受试者中，解释了很大一部分残余心血管风险。血管衰老加速的过程越来越被认为是炎症可能增加心血管疾病风险的潜在机制。反过来，细胞衰老代表了血管壁内炎症的一个重要来源，可能形成一个恶性循环，促进动脉粥样硬化的进展，而与个体心血管危险因素负担无关。在这篇综述中，我们总结了目前的证据，表明生物衰老在心血管疾病中的作用，以及炎症如何可能作为这种关联的关键介质。
