Inhibition of the VEGF receptor 2 combined with chronic hypoxia causes cell death‐dependent pulmonary endothelial cell proliferation and severe pulmonary hypertension

By L. Taraseviciene‐Stewart, Y. Kasahara, Lori Alger, P. Hirth, G. Mahon, J. Waltenberger, N. Voelkel, R. Tuder. The FASEB Journal, 2001

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Animal models of pulmonary arterial hypertension: the hope for etiological discovery and pharmacological cure. (2009, background): “They found that a VEGF receptor inhibitor, Sugen 5416 (SU-5416), caused mild PH and pulmonary vascular remodeling in normoxic rats but a severe, irreversible PH associated with precapillary arterial endothelial proliferation in chronically hypoxic rats (161).”
VEGF regulates haematopoietic stem cell survival by an internal autocrine loop mechanism (2002, background): “However, interference with this loop may, at least in part, be responsible for certain unexpected effects of small-molecule VEGFR kinase inhibitor”
Mechanisms of disease: pulmonary arterial hypertension (2011, background): “35, 36 However, when VEGFR inhibition is combined with chronic hypoxia in rats, severe pulmo nary hypertension with angioproliferative lesions develops, 37, 38 and when rats with established pulmonary hypertension are treated with VEGF, the disease is aggravated.”
Cellular and molecular pathobiology of pulmonary arterial hypertension. (2004, background): “Because endothelial cell death, cell proliferation, and the development of severe pulmonary hypertension could be blocked by a broad-spectrum caspase inhibitor, it appeared that the selection of an apoptosis-resistant endothelial cell phenotype might be the critical event responsible for pulmonary a”