Extracellular vesicles (EVs) play a crucial role in angiogenesis and modulating angiogenic signaling pathways. This review explores the diverse functions of EVs in blood vessel formation and their potential as therapeutic tools for both physiological and pathological conditions. EVs, including exosomes, microvesicles, and apoptotic bodies, are membrane-bound structures that carry proteins, lipids, and nucleic acids, enabling intercellular communication and influencing angiogenic processes. Exosomes, derived from endosomes, are small vesicles (40–150 nm) that contain a wide range of cargo, including microRNAs, which regulate angiogenesis. Microvesicles, produced by outward budding of the plasma membrane, and apoptotic bodies, formed from dying cells, also contribute to angiogenesis by delivering bioactive components to recipient cells. Angiogenesis, the process of new blood vessel formation, is essential for tissue development, wound healing, and disease progression. It involves two main mechanisms: sprouting angiogenesis, where endothelial cells sprout and extend toward angiogenic signals, and intussusceptive angiogenesis, where interstitial tissue invades preexisting vessels. Vascular endothelial growth factor (VEGF) is a key mediator of angiogenesis, promoting endothelial cell proliferation, migration, and vascular remodeling. Other factors, such as fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and angiopoietins, also play roles in angiogenesis. EVs from various cell types, including endothelial cells, mesenchymal stem cells, and cancer cells, have been shown to influence angiogenesis. MSC-derived EVs enhance angiogenesis by promoting the expression of pro-angiogenic factors and modulating signaling pathways such as Akt and ERK. EVs from cancer cells can promote tumor angiogenesis by supporting tumor cell proliferation and modifying the tumor microenvironment. EVs also have therapeutic potential in modulating angiogenesis for conditions such as heart disease, cancer, and ischemic injuries. Despite their promise, EV-based therapies face challenges, including the need for precise targeting and understanding of EV interactions. Further research is needed to fully elucidate the mechanisms by which EVs influence angiogenesis and to develop standardized methods for their therapeutic application. The potential of EVs as diagnostic and therapeutic agents in angiogenesis-related diseases is significant, with ongoing studies aiming to enhance their clinical utility.Extracellular vesicles (EVs) play a crucial role in angiogenesis and modulating angiogenic signaling pathways. This review explores the diverse functions of EVs in blood vessel formation and their potential as therapeutic tools for both physiological and pathological conditions. EVs, including exosomes, microvesicles, and apoptotic bodies, are membrane-bound structures that carry proteins, lipids, and nucleic acids, enabling intercellular communication and influencing angiogenic processes. Exosomes, derived from endosomes, are small vesicles (40–150 nm) that contain a wide range of cargo, including microRNAs, which regulate angiogenesis. Microvesicles, produced by outward budding of the plasma membrane, and apoptotic bodies, formed from dying cells, also contribute to angiogenesis by delivering bioactive components to recipient cells. Angiogenesis, the process of new blood vessel formation, is essential for tissue development, wound healing, and disease progression. It involves two main mechanisms: sprouting angiogenesis, where endothelial cells sprout and extend toward angiogenic signals, and intussusceptive angiogenesis, where interstitial tissue invades preexisting vessels. Vascular endothelial growth factor (VEGF) is a key mediator of angiogenesis, promoting endothelial cell proliferation, migration, and vascular remodeling. Other factors, such as fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and angiopoietins, also play roles in angiogenesis. EVs from various cell types, including endothelial cells, mesenchymal stem cells, and cancer cells, have been shown to influence angiogenesis. MSC-derived EVs enhance angiogenesis by promoting the expression of pro-angiogenic factors and modulating signaling pathways such as Akt and ERK. EVs from cancer cells can promote tumor angiogenesis by supporting tumor cell proliferation and modifying the tumor microenvironment. EVs also have therapeutic potential in modulating angiogenesis for conditions such as heart disease, cancer, and ischemic injuries. Despite their promise, EV-based therapies face challenges, including the need for precise targeting and understanding of EV interactions. Further research is needed to fully elucidate the mechanisms by which EVs influence angiogenesis and to develop standardized methods for their therapeutic application. The potential of EVs as diagnostic and therapeutic agents in angiogenesis-related diseases is significant, with ongoing studies aiming to enhance their clinical utility.