Inflammation induces endothelial-to-mesenchymal transition and promotes vascular calcification through downregulation of BMPR2.

ABSTRACT: Endothelial-to-mesenchymal transition (EndMT) has been unveiled as a common cause for a multitude of human pathologies, including cancer and cardiovascular disease. Vascular calcification is a risk factor for ischemic vascular disorders and slowing calcification may reduce mortality in affected patients. The absence of early biomarkers hampers the identification of patients at risk. EndMT and vascular calcification are induced upon cooperation between distinct stimuli, including inflammatory cytokines and transforming growth factor beta (TGF-β) family members. However, how these signaling pathways interplay to promote cell differentiation and eventually vascular calcification is not well understood. Using in vitro and ex vivo analysis in animal models and patient-derived tissues, we have i

SUBMITTER: Sanchez-Duffhues G 

PROVIDER: S-EPMC6590480 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature