Department of Cellular and Molecular Medicine, Cleveland Clinic Lerner Research Institute, 9500 Euclid Avenue, NC-10, Cleveland, Ohio 44195, USA.
Nat Rev Microbiol. 2018 Mar;16(3):171-181. doi: 10.1038/nrmicro.2017.149. Epub 2018 Jan 8.
Although diet has long been known to contribute to the pathogenesis of cardiovascular disease (CVD), research over the past decade has revealed an unexpected interplay between nutrient intake, gut microbial metabolism and the host to modify the risk of developing CVD. Microbial-associated molecular patterns are sensed by host pattern recognition receptors and have been suggested to drive CVD pathogenesis. In addition, the host microbiota produces various metabolites, such as trimethylamine-N-oxide, short-chain fatty acids and secondary bile acids, that affect CVD pathogenesis. These recent advances support the notion that targeting the interactions between the host and microorganisms may hold promise for the prevention or treatment of CVD. In this Review, we summarize our current knowledge of the gut microbial mechanisms that drive CVD, with special emphasis on therapeutic interventions, and we highlight the need to establish causal links between microbial pathways and CVD pathogenesis.
尽管饮食早已被认为是导致心血管疾病 (CVD) 的一个因素,但过去十年的研究揭示了营养摄入、肠道微生物代谢与宿主之间的一种意想不到的相互作用,这种相互作用可以改变发生 CVD 的风险。微生物相关的分子模式被宿主模式识别受体感知,并被认为可以驱动 CVD 的发病机制。此外,宿主微生物群产生各种代谢物,如三甲胺 N-氧化物、短链脂肪酸和次级胆汁酸,这些代谢物会影响 CVD 的发病机制。这些新的进展支持了这样一种观点,即针对宿主和微生物之间的相互作用进行靶向治疗可能有希望预防或治疗 CVD。在这篇综述中,我们总结了目前关于肠道微生物驱动 CVD 的机制的认识,特别强调了治疗干预措施,并强调了需要在微生物途径和 CVD 发病机制之间建立因果关系。