Pulmonary hypertension, primarily pulmonary arterial hypertension (PAH), is a life-threatening disease of the pulmonary vascular system with a progressive course. The patient dies as a result of right-sided heart failure in the final stage of the disease. The prognosis is poor because there is a lack of curative treatment options. Clinical and genetic studies discovered certain proteins, which are possibly related to PAH. One of these proteins was the angiopoietin-like 4 protein (Angptl4). Angptl4 is a circulating plasma protein structurally related to angiopoietins. It influences a large number of physiological and pathological processes in the organism. However, the exact impacts of Angptl4 on lung, heart and circulatory system are largely unknown. The experimental project of this dissertation included two sub-experiments. To induce PAH, the mouse hypoxia model was chosen in both sub-experiments. In the first subset of the experiment, recombinant Angptl4 was continuously administered via an osmotic minipump. With the help of imaging, hemodynamic and histological diagnostics, vascular remodeling in the lungs, changes in the lung parenchyma and impaired cardiac function could be determined in both the hypoxic and normoxic test groups. In the second subset of experiments, a neutralizing Angptl4 antibody was administered via intraperitoneal injections at regular intervals. Antibody treatment had significantly reduced remodeling in the pulmonary vasculature, but had no impact on the heart and its functionality. The negative impacts of the increased Angptl4 level on the pulmonary vessels and cardiac function confirm Angptl4 as a risk factor for PAH. Treatment with neutralizing antibodies offers a new therapeutic option to get closer to curing a previously incurable disease.