The vascular endothelium that lines the vascular intima is involved in various processes, including smooth muscle tension, host defense response, angiogenesis, and tissue fluid hemostasis . Phosphatase and tensin homolog(PTEN) is required for adequate cardiovascular homeostasis. It may be involved in angiogenesis and vascular integrity regulation . PTEN is a tumor suppressor gene demonstrated to be critical for the proliferation of vascular smooth muscle cells (SMC). It is a possible therapeutic target for vascular remodeling . The Notch-PTEN signaling axis is identified as the coordinator of blood vessel density, implying that the PTEN-APC/C-Fzr1/Cdh1 hub participates in angiogenesis . PTEN mutation carriers exhibit vascular problems. In patients with PTEN mutations, vascular abnormalities typically manifest as a multifocal intramuscular mix of rapid flow channels and ectopic fat . Increased PTEN expression limits the growth of vascular smooth muscle cells and arterial restenosis . PTEN also plays a critical role in differentiating vascular smooth muscle cells (SMCs) . PTEN is an anti-inflammatory and anti-fibrotic protein that is required for SMC differentiation to occur . SMC deficiency in PTEN results in pathological artery remodeling . Cardiovascular development during embryonic development and postnatal neovascularization are intricate processes that share signaling molecules . PTEN reduces vascular germination and endothelial tube formation generated by VEGF in vitro; a dominant-negative mutation of PTEN abolishes these effects . PTEN has a role in cardiovascular development and angiogenesis by regulating the production of vascular signaling molecules such as VGF .Mutations in these molecules result in abnormalities in cardiovascular development . Beside, PTEN promotes late endosomal maturation via its protein phosphatase activity. It inhibits epidermal growth factor receptor (EGFR) signaling . PTEN deficiency affects ligand-bound EGFR's passage from early to late endosomes .