Grant: Operating Grant

The formation of new blood vessels termed angiogenesis in an uncontrolled and overexcessive manner occurs in the setting of diseases such as atherosclerosis, tumor growth and metastasis, ocular diseases, arthritis and psoriasis. These new blood vessels provide the circuitry to bring inflammatory cells and nutrients to support (feed) the pathological milieu, and thus, favoring the progression of the disease. Consequently, our general hypothesis is that the inhibition of pathological angiogenesis (consisting on the blockade formation of undesired new blood vessels) could be a potential therapeutic approach to circumvent the development or the progression chronic diseases. The induction of pathological angiogenesis requires the contribution of inflammatory cells and the contribution of specific proteins (termed growth factors). One of these growth factors is the protein VEGF, which induces an acute inflammatory response, and acting as a leading promoter in the initiation of angiogenesis. During the last years, we discovered how VEGF is inducing the inflammatory response. In our recent studies, we also studied another family of growth factors (namely the angiopoietins; Ang1 and Ang2), which are also involved in blood vessels formation. In addition, they can also activate inflammatory circulating blood cells like the neutrophils, which can promote inflammatory biological activities, an initial key event in the induction of pathological angiogenesis. Thus, our research team is trying to understand how these growth factors (e.g. VEGF and the angiopoietins) are inducing an inflammatory response, namely following the activation of the neutrophils, and what could be the beneficial effect to prevent the participation of these growth factors and the inflammatory cells in the formation of non-desired blood vessels in pathological diseases.