Interstitial lung diseases (ILD) constitute a large group of disorders characterized by various etiology and pathogenesis. Inflammation and pulmonary fibrosis are the most important processes in the course of ILD. Disease causes the decrease of the gas diffusion in the lungs and provokes hypoxia. Chronic inflammation and hypoxia are strong stimulus of neovascularization. Neoangiogenesis is a principal response of vessels to inflammation. The critical importance of tumor angiogenesis in the development and metastatic spread of tumors is proved. Relations of ILD with neoplasma have been observed. Neovascularization takes an important role in wound healing allowing the cells to flow into damaged structures. Recently, pulmonary fibrosis has been deemed to result from abnormal wound healing in the lung in response to injury to the alveolar epithelium. Angiogenesis participates in pathogenesis of idiopathic pulmonary fibrosis. More and more data suggest the role of angiogenesis in pathogenesis of other ILDs, such as granulomatosis, fibrosis and vasculitis. The mechanism of angiogenesis in ILD is not clear yet. New data concerning participation of neoangiogenesis in pathogenesis of ILD created target for new drugs. Thalidomide, a strong antiangiogenic drug was used successfully in the some cases of ILD.