EDITOR'S CHOICE The haematopoietic stem cell niche: a new player in cardiovascular disease? https://doi.org/10.1093/cvr/cvy308 Published: 24 December 2018 Article history PDF Cite Permissions cardiovascular diseases hematopoiesis hematopoietic stem cells hematopoietic system Issue Section: Reviews 1. Introduction The haematopoietic system is responsible for the production and maintenance of all blood cells within the body. This ranges from pluripotent haematopoietic stem and progenitor cells (HSPCs) through to mature fully differentiated leucocytes, erythrocytes, and platelets. The influence of the haematopoietic system on the progression of many diseases has been a topic of great interest throughout the last half century. In particular, the role that the mature immune cell compartment of the haematopoietic system plays in onset of disease, for example systemic inflammation and autoimmune disorders have received much attention. White blood cells, both of the innate and adaptive immune system, are implicated in both the exacerbation and resolution of inflammation. The dynamic nature of the white blood cell populations has generated significant interest into how inflammation can be regulated by modulation of immune cell function. In the setting of cardiovascular disease (CVD), it is now established that elevated numbers of circulating innate immune cells are strong predictors of atherosclerotic progression and cardiovascular events.View largeDownload slide Influence of the haematopoietic system on cardiovascular disease. The diagram represents a cycle of inflammation driven by immune cells. Within the BM, the site of primary haematopoiesis, the HSPCs begin to cycle and mobilize to the spleen. In the spleen, the HSPCs proliferate and differentiate into the downstream myeloid cells such as monocytes. The monocytes produced in the spleen are released into circulation, under the inflammatory conditions these splenic monocytes are particularly atherogenic. At the same time monocyte populations from the BM are released into the circulation. The circulating monocytes can then reach the site of arterial plaque formation, infiltrate the lesion, form macrophages, and propagate the inflammation. With an increase in atherogenesis and plaque instability the lesion may rupture, which is the major cause of myocardial infarction and stroke. Inflammatory signals from the infarcted heart and the plaque can return to the BM where they further exacerbate the haematopoietic dysfunction.
