Figure 3.

Schematic representation highlighting the potential protective roles of Ang2 in HGPS across various tissues. This figure illustrates the diverse protective effects of Ang2 in multiple tissues affected by HGPS. Ang2 may exert atheroprotective effects by increasing NO production, reducing LDL oxidation, and decreasing macrophage accumulation. In the context of endothelial dysfunction, Ang2 has the potential to reverse dysfunction through increased vasculogenesis, improved NO mechanosensing production, and reduced inflammation. In the cardiovascular system, Ang2 may improve cardiac remodeling and cellular dynamics, promoting neovascularization and better regulation of heart development. Furthermore, Ang2 could enhance lymphatic integrity by reducing fibrosis, supporting thymocyte development, and improving cell proliferation, vascular smooth muscle cell (VSMC) recruitment, and vascularization. In white adipose tissue (WAT), Ang2 may improve homeostasis through adipose tissue remodeling, adipocyte differentiation, and enhancing metabolic health, while reducing fibrosis and inflammation. For bone tissue, Ang2 has the potential to promote wound healing by activating autophagy, reducing inflammation, and improving vascularization, which supports the balance between bone formation and resorption. Additionally, Ang2 can enhance blood flow recovery by promoting arteriogenesis and improving the interaction between ECs and VSMCs, strengthening structural integrity and adaptability to hypoxic conditions. In the brain, Ang2 has been shown to improve vascular integrity, increase neurogenesis, promote neuroblast migration, and enhance blood flow, supporting tissue recovery in neurovascular pathology. This figure was created using BioRender.