Biasucci Luigi M, La Rosa Giulio, Pedicino Daniela, D'Aiello Alessia, Galli Mattia, Liuzzo Giovanna
Department of Cardiovascular Science, Catholic University of Sacred Heart, Largo Agostino Gemelli 8, 00168, Rome, Italy.
Curr Cardiol Rep. 2017 Sep;19(9):84. doi: 10.1007/s11886-017-0896-0.
This review focuses on the complex relationship between inflammation and the onset of acute coronary syndrome and heart failure.
In the last few years, two important lines of research brought new and essential information to light in the pathogenesis of acute coronary syndrome: a) the understanding of the immune mediate mechanisms of inflammation in Ischemic Heart Disease (IHD) and b) evidence that the inflammatory mechanisms associated with atherosclerosis and its complications can be modulated by anti-inflammatory molecules. A large amount of data also suggests that inflammation is a major component in the development and exacerbation of heart failure (HF), in a symbiotic relationship. In particular, recent evidence underlies peculiar aspects of the phenomenon: oxidative stress and autophagy; DAMPS and TLR-4 signaling activation; different macrophages lineage and the contribution of NLRP-3 inflammasome; adaptive immune system. A possible explanation that could unify the pathogenic mechanism of these different conditions is the rising evidence that increased bowel permeability may allow translation of gut microbioma product into the circulation. These findings clearly establish the role of inflammation as the great trigger for two of the major cardiovascular causes of death and morbidity. Further studies are needed, to better clarify the issue and to define more targeted approaches to reduce pathological inflammation while preserving the physiological one.
本综述重点关注炎症与急性冠状动脉综合征及心力衰竭发病之间的复杂关系。
在过去几年中，两条重要的研究路线为急性冠状动脉综合征的发病机制带来了新的重要信息：a）对缺血性心脏病（IHD）中炎症的免疫介导机制的理解；b）有证据表明与动脉粥样硬化及其并发症相关的炎症机制可被抗炎分子调节。大量数据还表明，炎症在心力衰竭（HF）的发生和加重中起主要作用，二者存在共生关系。特别是，最近的证据揭示了该现象的一些特殊方面：氧化应激与自噬；损伤相关分子模式（DAMPs）与Toll样受体4（TLR-4）信号激活；不同的巨噬细胞谱系以及NLRP-3炎性小体的作用；适应性免疫系统。一个可能统一这些不同病症致病机制的解释是，越来越多的证据表明肠道通透性增加可能使肠道微生物群产物进入循环。这些发现明确了炎症作为导致两大主要心血管疾病死亡和发病的重要触发因素的作用。需要进一步研究，以更好地阐明这一问题，并确定更有针对性的方法来减少病理性炎症，同时保留生理性炎症。
