Age-related physical changes, such as low-grade inflammation and increased oxidative stress, induce endothelial repair and cause active arterial wall thickening by stimulating the production of CD34+ cells (the principal mediators of atherosclerosis). Despite this, aggressive endothelial repair (progressing atherosclerosis) might cause a wasting reduction in CD34+ cells, which could result in a lower capacity of endothelial repair and hypertension. As yet, no prospective study has clarified the association of circulating CD34+ cells with active arterial wall thickening. We conducted a prospective study of 363 men aged 60-69 years who participated in a general health checkup at least twice from 2014-2017. The circulating CD34+ cell count was significantly positively associated with active arterial wall thickening among subjects without hypertension (n = 236), but not among subjects with hypertension (n = 127). The fully adjusted odds ratios (ORs) of active arterial wall thickening for the logarithmic circulating CD34+ cell count were 1.83 (1.19, 2.84) and 0.69 (0.36, 1.32) for subjects without and with hypertension, respectively. Circulating CD34+ cells are positively associated with active arterial wall thickening in subjects without hypertension. this study demonstrates a means to clarify the mechanisms of endothelial repair in elderly subjects. Recently, bone marrow-derived hematopoietic stem cells (immature cells, such as CD34+ cells) have been revealed to play a major role in vascular homeostasis 1-3. It is likely that the number of circulating CD34+ cells could indicate the capacity of endothelial maintenance 4-6. However, it is known that hematopoietic bone marrow activity declines with age 7-10 , which might induce a lower capacity of endothelial maintenance in elderly subjects. Furthermore, aging is a well-known cause of endothelial injury 11,12 which subsequently induces endothelial repair. In addition, the aggressive endothelial repair that causes atherosclerosis might induce a wasting reduction of circulating CD34+ cells 6,13 which result in a shortage of the mediators of endothelial repair. Moreover, inadequate endothelial repair might cause hypertension in elderly individuals 14. These previous studies indicate that there are close connections among the age-related decline of bone marrow activity, age-related endothelial injury, and the wasting reduction of circulating CD34+ cells. Platelets are also known to play an important role in vascular inflammation and vessel wall remodeling 15,16. Indeed, platelets promote the mobilization of bone marrow-derived CD34+ cells into the peripheral blood 17-21 , and CD34+ cells also induce platelet elevation 22,23. Furthermore, platelets have been reported to play an important role in the initial development of atherosclerotic lesions 24 , and not only induce the differentiation of human CD34+ cells into endothelial cells, but also into foam cells, which contribute to the development of atherosclerosis 25. Therefore, platelets also play an important role in the a...