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Cathepsin B expression is associated with arterial stiffening and atherosclerotic vascular disease

Accumulating evidence supports the interaction among vascular aging, inflammation and atherosclerosis. Therefore, exploring underlying pathophysiology may highlight key linking pathways that could be targeted for intervention. Cathepsin B (CTSB), a proteolytic enzyme mainly located in lysosomes and endosomes, can be activated and released by ageing-associated cell acidification. CTSB may also be involved in arterial degeneration, calcification and arterial stiffening by augmenting inflammatory load and by degradation of the elastin-containing arterial extracellular matrix. CTSB is also highly expressed in human carotid plaques and correlates with plaque severity and symptomatic events. Thus, experimental evidence supports a central role of CTSB in ageing processes, atherogenesis and its consequences. However, its clinical role in atherosclerotic cardiovascular disease (ASCVD) has not been sufficiently explored, while its association with vascular aging is unknown. CTSB expression in peripheral blood mononuclear cells (PBMCs) was measured in 224 consecutive subjects (148 without clinically overt coronary artery disease (CAD) (control group), 46 with stable CAD and 30 with acute myocardial infarction (AMI)) using quantitative SYBR Green real-time polymerase chain reaction. Participants underwent peripheral vascular assessment by measurement of aortic stiffness using pulse wave velocity (PWV) (Complior, Artech Medical Saint Quentin Fallavier, France) and by documentation of carotid and femoral atherosclerotic plaques using high-resolution B-mode ultrasound imaging (14.0-MHz multifrequency linear-array probe, Vivid 7 Pro, General Electric Boston, United States). All subjects provided written consent for participation in the study. CTSB in the highest tertile was associated with older age, higher prevalence of arterial hypertension, hyperlipidaemia and with lower estimated glomerular filtration rate (p< 0.05 for all). Overall, CAD patients presented higher CTSB expression than controls (p1⁄4 0.006) (Figure 1). Comparisons by subgroups of CAD showed that AMI patients had increased CTSB expression compared to control subjects (p1⁄4 0.007), while stable CAD and AMI patients did not differ (p1⁄4 0.154). In addition, in control subjects but not in CAD patients, CTSB in the highest tertile presented fourfold increased odds for higher PWV after adjustment for traditional CAD risk factors (TRFs) and renal function (Table 1, Figure 1). CTSB levels were also independently associated with the number of CAD arteries after adjustment for TRFs and renal