Following on from a previous finding that there was a significant association between the increase in inflammatory monocytes after AMI and microcirculation impairment, and another that direct rennin inhibitors mediate the suppression of inflammatory monocytes after AMI to improve myocardial relief rate, the researchers are setting out to: discover the significance of peripheral blood monocytes in microcirculation impairment; clarify the influence of renin/aldosterone (the renin-angiotensin-aldosterone system is the most important system involved in the regulation of systemic blood pressure, renal blood flow, and monocytes recruitment); and establish a treatment. Initially, the team conducted clinical research involving 50 patients with AMI, as well as basic research involving an experimental animal model that will enable the team to examine the effect of various drugs on microcirculatory impairment and monocyte subset. The researchers then worked to compare and examine the relationship between the quantitative and qualitative changes of the monocyte subset and the microcirculatory disorder and the characteristics of the intracoronary lesion for 50 patients with myocardial infarction, as well as evaluating the influence of various drugs. They also used the myocardial infarction model to investigate the influence of various drugs on the degree of microcirculatory impairment in wild type mouse and each knockout mouse, its molecular mechanism, and the quantitative and qualitative change of the monocyte subset. In their project ‘Association between P-selectin glycoprotein ligand-1 and pathogenesis in ACS assessed by optical coherence tomography’, the researchers set out to shed light on how up-regulation of monocyte subsets leads to coronary plaque rupture followed by thrombus formation. To do so, they enrolled 100 individuals – patients with myocardial infarction, unstable angina pectoris, or stable angina pectoris who underwent coronary angiography, as well as control subjects. The researchers used flow cytometry to measure three monocyte subsets (CD14++CD16-CD14++CD16+, and CD14+CD16+) and the expression of P-selectin glycoprotein ligand-1 (PSGL-1) and found that circulating peripheral CD14++CD16+ monocytes expressed PSGL-1 more frequently than CD14++CD16- and CD14+CD16+ monocytes in patients with ACS.