Angiogenesis and signal transduction mechanisms are two hot research areas at present. In recent years, important progress has been made in the study of pro-angiogenic mediators and their signal transduction mechanisms in vascular endothelial cells. At present, angiogenesis research mainly involves two disciplines, namely, tumor and cardiovascular, and is particularly well studied in tumor. Tumor angiogenesis is a more mature pathogenesis, and the signal transduction mechanism is also clearer, in which MAPK family is considered as an important member of angiogenic signaling pathway, with different functions of regulating cell growth and differentiation. The signal transduction mechanism in cardiovascular diseases, especially in myocardial ischemia, has been little studied, especially the signal transduction mechanism of beneficial Qi and blood activating herbs to improve the function of ischemic myocardium and promote vascular renewal has been even less reported. The MAPK family is divided into three subclasses: ERKl/2, JNK, and p38MAPK. ERKl/2 signaling pathway is activated by growth factors; while JNK pathway and p38/HOG-1 pathway, which are activated by UV light, osmolarity changes, cytokines (IL-1), TNF, and physiological stress, are collectively called MAPK stress signaling pathway. A large number of previous studies have confirmed that cytokines such as VEGF, FGF, PDGF, and EGF mediate cell proliferation mainly through the mitogen-activated protein kinase signaling pathway. However, an increasing number of studies have found that many growth factors produced by hypoxia induction can mediate vascular smooth muscle cell (VSMC) proliferation through the PI3K pathway and that MAPK can act as a target molecule downstream of PI3K to regulate cell proliferation through the PI3K/ MAPK pathway. PI3K is a key signaling molecule in many life activities, and PI3K-mediated signal transduction pathways regulate cell division, differentiation, and apoptosis. When PI3K is activated by growth factors binding to cell membrane receptors, phosphorylation of the 3rd light group in the inositol ring on the cell membrane produces 3-PIP, 3,4-PIP2 and 3,4,5-PIP3, and these products can act as second messengers to their downstream proteins or kinases closely related to cell growth, such as AKT, which eventually activate and upregulate cyclinD1 to cause cell proliferation. AKT is of increasing interest for its involvement in signaling processes mediated by growth factor activation via P13K. PKB expression can induce neovascularization in areas of ischemia and has recently been shown to maintain the integrity of damaged myocardial tissue and mediate signaling pathways. AKT is a direct target protein downstream of PI3K. various growth factors such as PDGF can induce PKB activation through phosphorylation of tyrosine (Y740/Y751) sites on the PDGF receptor to produce a high affinity site for binding to the p85 subunit of PI3 K. In addition, since the p110 subunit of PI3K can also interact directly with the small molecule GTPase Ras, activated Ras can also partially activate PKB through PI3K. pKB can also act directly on the nuclear transcription factor CREB through an intranuclear signaling pathway to cause the expression of specific genes. pKB activated by PI3K can mediate the activation of various growth factors such as PDGF, EGF insulin, thrombin dGF-1 and NGF induced cell growth. The results of the present experiment showed that the Chinese herbal medicine Angelica tonic blood soup could promote the expression of VEGF in the ischemic area; at the same time, it promoted the expression of PI3K to different degrees, which had a significant advantage over the model group and the betalactone group. Through the pro-expression effect on PI3K, the activation of downstream signaling pathways was further initiated. The AKT protein expression was significantly promoted in the mid-dose group of Betalac and Angelica Blood Tonic, while the MAPK protein expression was significantly activated in the model group and the small-dose group of Angelica Blood Tonic. Through the above pathways, VEGF protein expression in the ischemic region of myocardium was finally enhanced, producing an angiogenic effect in the ischemic region. This indicates that Yi Qi and Blood activating herbs carry out anti-ischemic-hypoxic and pro-angiogenic effects from different pathways. Also ischemia-hypoxia is an important signaling initiation mechanism, which was shown to have a more pronounced effect in the experiment. It has been confirmed that beneficial qi and blood activating drugs have the effect of improving human immunity and enhancing self-repair ability. Our group’s previous study also showed that the beneficial qi and blood invigorating herbal medicine Angelica tonic blood soup can improve myocardial ischemia and promote angiogenesis. Under the stimulation of ischemia and hypoxia, myocardial cells and vascular endothelial cells suffer damage, and the body initiates protective mechanisms to ameliorate the damage by promoting cell increase and vascular increase, but the local but emergency response cannot save the large area of damage. By regulating cellular signaling mechanisms and initiating growth and proliferation signals to promote neovascularization, beneficial qi and blood-boosting drugs enhance the body’s resistance to repair and can be expected to cooperate with the response to damage that exceeds the ability to repair itself. The study of new angiogenic factors and their signaling mechanisms is not only a basic topic in developmental biology and cell biology, but also has important clinical significance, and it can be said that most human diseases are related to blood circulation and neoangiogenesis. However, whether the promotion and inhibition of angiogenesis affects tumor regression and at the same time the maturation of ischemic myocardial collateral is still a difficult research problem. Although these studies are still relatively preliminary, they are progressing rapidly and will certainly provide some new ideas for the effective treatment of many diseases.