The role of hydrogen sulphide (H2S) in angiogenesis has been widely demonstrated. Vascular endothelial growth factor (VEGF) plays an important role in H2S‐induced angiogenesis. H2S promotes angiogenesis by upregulating VEGF via pro‐angiogenic signal transduction. The involved signalling pathways include the mitogen‐activated protein kinase pathway, phosphoinositide‐3 kinase pathway, nitric oxide (NO) synthase/NO pathway, signal transducer and activator of transcription 3 (STAT3) pathway, and adenosine triphosphate (ATP)‐sensitive potassium (KATP) channels. H2S has been shown to contribute to tumour angiogenesis, diabetic wound healing, angiogenesis in cardiac and cerebral ischaemic tissues, and physiological angiogenesis during the menstrual cycle and pregnancy. Furthermore, H2S can exert an anti‐angiogenic effect by inactivating Wnt/β‐catenin signalling or blocking the STAT3 pathway in tumours. Therefore, H2S plays a double‐edged sword role in the process of angiogenesis. The regulation of H2S production is a promising therapeutic approach for angiogenesis‐associated diseases. Novel H2S donors and/or inhibitors can be developed in the treatment of angiogenesis‐dependent diseases. Hydrogen sulphide and nitric oxide interact and depend on each other to jointly regulate angiogenesis.