Fig. 3: Arginase promotes various CVDs through regulating cellular functions and endothelial dysfunction.

Arginase can promote CF proliferation and contribute to cardiac remodeling, which plays a crucial role in heart failure. ARG2 expression can induce the VSMCs proliferation, a hallmark characteristic of hypoxia-induced PAH. Furthermore, upregulated arginase induces endothelial dysfunction via NO reduction and ROS production, which promotes the development of a variety of CVDs such as hypertension, diabetic vascular disease, ischemic reperfusion and atherosclerosis. Moreover, ARG2 leads to atherosclerotic plaque instability through promoting VSMC senescence and apoptosis and dampening endothelial autophagy in atherosclerosis. ARG2 expression triggers macrophage pro-inflammatory responses, resulting in the development of atherosclerosis. CVDs cardiovascular diseases, CF cardiac fibroblast, VSMC vascular smooth muscle cell, EC endothelial cell, PAH pulmonary arterial hypertension, NO nitric oxide, ROS reactive oxygen species.