The vasculature of the kidney is a heterogeneous structure, whose functional integrity is essential for the regulation of renal function. Owing to the importance of the endothelial cells in vascular biology, chronic endothelial alterations are susceptible to impair multiple aspects of renal physiology and, in turn, to contribute to renal fibrosis. Although systemic endothelial dysfunction is undoubtedly associated with chronic kidney disease, the role of the renal endothelium in the initiation and the progression of renal fibrosis remains largely elusive.
My main research topic is to analyze the role of renal endothelial alterations in the progression of fibrosis in chronic kidney disease. More specifically, we are currently focusing on the implications of renal endothelial dysfunction in the regulation of local hemodynamics and inflammation in hypertension-associated kidney disease. The evaluation of promising therapeutic strategies targeting renal endothelial alterations during the initiation and the progression of renal fibrosis is a major objective of our ongoing work.